The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index; 15 of the 25 sources its claims cite were checked for support.
TREM2 Modulation Remodels the Tumor Myeloid Landscape Enhancing Anti-PD-1 Immunotherapy
Open accessAbstract
SUMMARY Checkpoint immunotherapy unleashes T cell control of tumors, but is undermined by immunosuppressive myeloid cells. TREM2 is a myeloid receptor that transmits intracellular signals that sustain microglial responses during Alzheimer’s disease. TREM2 is also expressed by tumor-infiltrating macrophages. Here, we found that Trem2−/− mice are more resistant to growth of various cancers than wild-type mice and are more responsive to anti-PD-1 immunotherapy. Furthermore, treatment with anti-TREM2 mAb curbed tumor growth and fostered regression when combined with anti-PD-1. scRNA-seq revealed that both TREM2 deletion and anti-TREM2 are associated with scant MRC1+ and CX3CR1+ macrophages in the tumor infiltrate, paralleled by expansion of myeloid subsets expressing immunostimulatory molecules that promote improved T cell responses. TREM2 was expressed in tumor macrophages in over 200 human cancer cases and inversely correlated with prolonged survival for two types of cancer. Thus, TREM2 might be targeted to modify tumor myeloid infiltrates and augment checkpoint immunotherapy.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
TREM2 deficiency or anti-TREM2 antibody treatment restricts tumor growth and strongly enhances anti-PD-1 immunotherapy in mouse sarcoma and colorectal cancer models. TREM2 marks tumor-infiltrating macrophages in over 200 human cancers and correlates with worse survival in colorectal carcinoma and triple-negative breast cancer.
Key findings
- Trem2−/− mice were more resistant than WT mice to MCA/1956 sarcoma, MC38 colorectal cancer, and PyMT mammary tumors; with suboptimal anti-PD-1 started on day 8, 40% of WT mice rejected MCA/1956 versus 100% of Trem2−/− mice, and all Trem2−/− mice controlled MC38 growth versus only a few WT mice.
- Anti-TREM2 mAb 178 alone gave significant but incomplete tumor control, while anti-TREM2 plus suboptimal anti-PD-1 conferred complete tumor control in all mice tested; anti-TREM2 treatment attenuated tumor growth more than Trem2 deficiency, and did not further attenuate growth in Trem2−/− mice.
- scRNA-seq showed that TREM2 deletion and anti-TREM2 treatment reduced MRC1+ and CX3CR1+ macrophage subsets and expanded immunostimulatory myeloid subsets; anti-TREM2 induced de novo Nos2-Macs-t and reduced Mrc1-Macs-t, Cycling-Macs-t, and Macs1-t.
- TREM2 was expressed in tumor macrophages in over 200 human cancer cases, including 75% of carcinomas in a 126-sample tissue microarray and virtually all 99 whole tumor sections; TREM2 expression inversely correlated with overall survival in CRC and with overall and relapse-free survival in TNBC.
Methods
- Mouse tumor models included MCA/1956 sarcoma, MC38 colorectal cancer, and PyMT mammary tumors in WT and Trem2−/− mice, with anti-PD-1, Fc-mutated anti-TREM2 mAb 178, control antibodies, CD4/CD8 depletion, flow cytometry, immunofluorescence, and ex vivo T cell cytokine analysis.
- scRNA-seq was performed on live CD45+ cells sorted from MCA/1956 tumors at day 10; genotype comparison averaged 19,758 cells with 13,545 UMI per cell, and antibody-treatment comparison averaged 2,726 cells per condition with 14,622 UMI per cell, analyzed with Seurat and UMAP.
- Human analyses used FFPE tissues including a multi-tumor tissue microarray of 126 samples, primary carcinomas (n = 99), tumor-draining lymph nodes (n = 33), and distant metastases (n = 12), plus TCGA survival and correlation analyses.
Limitations
- The paper states that mechanisms by which TREM2 deficiency and anti-TREM2 treatment impact tumor macrophages remain unclear, that future biochemical experiments are needed, and that variability was noted in T cell expansion and effector function between Trem2−/− and anti-TREM2-treated mice.
- The paper states that the anti-PD-1 regimen used was suboptimal and initiated late, and that TREM2’s survival association was not significant in other tumor types, suggesting context specificity.
- Evident from the text: several experiments were performed once or with small n, scRNA-seq used n = 2 per condition in one experiment, and human evidence is largely IHC/correlation without functional validation; combined anti-TREM2 plus anti-PD-1 cleared tumors, so no infiltrate could be analyzed in that group.
Model-written summary. Check it against the paper before relying on it.
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Cites
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Verification
Claims the paper makes
15 of 25 cited sources checked · 5 supported · 0 flagged · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Trem2−/− macrophages were shown to present antigens to T cells more effectively than WT macrophages in vitro (Ito and Hamerman, 2012).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > DISCUSSION
What the sources say
- Partly supportedcites Ito and Hamerman, 2012 sourceExperimental — accuracy not yet measured
The Results section (“TREM-2 negatively regulates antigen-specific T cell proliferation by BMDCs”; page unavailable) reports that TREM-2-deficient bone-marrow-derived dendritic cells induced more antigen-specific T-cell division than WT dendritic cells in vitro. The cited experiment did not test macrophages, so the claim attributes the finding to the wrong cell type. (LLM, conf=0.89)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“We have previously shown that TREM2 cooperates with CSF-1 in sustaining macrophage proliferation and survival (Ulland et al., 2017).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > DISCUSSION
What the sources say
- Partly supportedcites Ulland et al., 2017 sourceExperimental — accuracy not yet measured
The Results section on macrophage mTOR signaling shows that TREM2-deficient bone marrow-derived macrophages have impaired mTOR signaling and increased autophagy when CSF1 is limiting. The Discussion says TREM2-supported mTOR signaling promotes survival and proliferation in microglia, but the cited passages do not establish that TREM2 cooperates with CSF1 to sustain macrophage proliferation and survival. (LLM, conf=0.82)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“We have previously shown that TREM2 is induced in human monocytes and mouse bone marrow cells upon exposure to GM-CSF and CSF-1 (Bouchon et al., 2001; Turnbull et al., 2006).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > DISCUSSION
What the sources say
- Partly supportedcites Bouchon et al., 2001 sourceExperimental — accuracy not yet measured
The Results section on immature monocyte-derived dendritic cells reports high TREM-2 expression after human monocytes were cultured with GM-CSF and IL-4. It does not report induction in mouse bone marrow cells or by CSF-1; in fact, TREM-2 was undetectable in human monocyte-derived macrophages cultured with M-CSF. No page number is available in our copy. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites Turnbull et al., 2006 source
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We also re-clustered lymphoid cells, revealing heightened expression of activation markers, such as IFNγ and PD-1 (Pdcd1), by T cells and NK cells in Trem2−/− MCA tumors (Figures S2F–S2I).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Lack of TREM2 Impacts Tumor Myeloid and Lymphoid Landscape
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“TREM2 expression inversely correlated with overall survival and relapse in these cancer patients.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > DISCUSSION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“PD-1+ CD4 T cells were only increased in Trem2−/− mice treated with anti-PD-1 (Figure 4F).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > TREM2 Deficiency Enhances Checkpoint Blockade
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“On the other hand, the Macs1-g cluster, which expressed genes previously associated with IFN-γ imprinting and immunostimulation (Cxcl9 and Cd83) was much more predominant in Trem2−/−MCA tumors.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Lack of TREM2 Impacts Tumor Myeloid and Lymphoid Landscape
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Once again, tumor growth was more limited in Trem2−/− mice than in WT mice (Figures S1G and S1H).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > TREM2 Deficiency Delays Growth of Transplanted Tumors and Modifies Tumor-Immune Infiltrate
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“however, the relative proportion of a Ly6C+MHCIIlow/− subset was significantly reduced in the Trem2−/− infiltrates (Figure 1C)”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > TREM2 Deficiency Delays Growth of Transplanted Tumors and Modifies Tumor-Immune Infiltrate
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Interestingly, tumor growth was more attenuated in anti-TREM2-treated mice than in Trem2−/− mice (Figure 5C).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Anti-TREM2 Treatment Is Protective in the Sarcoma Model
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- Probably not a substantial claim. 19
- It may state two separate claims as one. 27
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“TREM2 is an activating receptor of the Ig-superfamily that binds lipids and transmits intracellular signals through the adaptor DAP12 (Peng et al., 2010; Ulland et al., 2017).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > INTRODUCTION
What the sources say
- Partly supportedcites Peng et al., 2010 sourceExperimental — accuracy not yet measured
The Introduction identifies TREM2 as an immunoglobulin-like, DAP12-associated receptor, and the Discussion describes signaling through the TREM2–DAP12 pathway. The Discussion says specific endogenous ligands for TREM2 were not yet known; this paper does not establish that TREM2 binds lipids. Page numbers are unavailable in our copy. (LLM, conf=0.89)
- Partly supportedcites Ulland et al., 2017 sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) says TREM2 recognizes phospholipids and transmits intracellular signals through DAP12 and DAP10; the Discussion describes it as an innate immune receptor involved in signaling. Our copy does not identify TREM2 as a member of the Ig-superfamily, so that part of the attributed description is unsupported. (LLM, conf=0.87)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In the liver, a TREM2+CD9+ subset of macrophages that differentiate from circulating monocytes expands during liver cirrhosis and contributes to fibrosis (Ramachandran et al., 2019).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > INTRODUCTION
What the sources say
- Supportedcites Ramachandran et al., 2019 source
The Results section, under “Pro-fibrogenic phenotype of scar-associated macrophages,” states that TREM2+CD9+ macrophages derive from recruited circulating monocytes and have a pro-fibrogenic phenotype. The Results also report that these cells expand in cirrhotic livers and promote collagen expression by hepatic stellate cells. Page numbers are not provided in the supplied passages. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In the adipose tissue, TREM2 sustains the presence of a population of lipid-associated macrophages (LAMs) that prevent the dysmetabolism engendered by a high-fat diet (Jaitin et al., 2019).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > INTRODUCTION
What the sources say
- Supportedcites Jaitin et al., 2019 source
The Results section on adipose tissue macrophage remodeling reports that, after high-fat-diet feeding, Trem2-deficient mice failed to accumulate LAMs. The Results section on metabolic homeostasis reports adipocyte hypertrophy, glucose intolerance, and other metabolic abnormalities in those mice; the Discussion says Trem2-driven LAM formation prevents adipocyte hypertrophy and loss of systemic lipid homeostasis under obese conditions. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“TREM2+ macrophages have also been reported in tumors (Lavin et al., 2017; Song et al., 2019), but the impact of TREM2 in tumor immune responses has not been addressed.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > INTRODUCTION
What the sources say
- Supportedcites Lavin et al., 2017 source
The Results section, under “Paired immune cell mapping reveals a distinct macrophage signature in lung adenocarcinoma,” identifies TREM2 as up-regulated in a tumor-associated macrophage cluster. This supports the cited claim that TREM2+ macrophages have been reported in tumors; the sentence’s separate statement about their impact is not attributed to this source. (LLM, conf=0.93)
- Supportedcites Song et al., 2019 source
The Discussion (page not provided) reports TREM2 among the genes upregulated during the monocyte-to-M2 macrophage transition within the intratumoral myeloid population. This supports the cited claim that TREM2+ macrophages have been reported in tumors. (LLM, conf=0.93)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“DAP12 recruits the protein tyrosine kinase Syk, which initiates a cascade of tyrosine phosphorylation events that activate downstream mediators such as PLCγ2, PI-3K, Vav, mTOR, and MAPK, ultimately leading to cell activation (Peng et al., 2010; Ulland et al., 2017).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > INTRODUCTION
What the sources say
- Partly supportedcites Peng et al., 2010 sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) describes a TREM2–DAP12 signaling complex containing Syk and PI3K p85, and reports activation of PLC-γ2, Vav3, and ERK1/2, a MAPK, in pathways involved in cell activation. It does not identify mTOR as a downstream mediator or establish the entire sequence as a Syk-initiated phosphorylation cascade. (LLM, conf=0.88)
- Partly supportedcites Ulland et al., 2017 sourceExperimental — accuracy not yet measured
The Introduction states that TREM2-associated DAP12 recruits Syk, while DAP10 recruits PI3-K. The Results link TREM2 signaling to PI3-K and mTOR, but the cited passages do not establish the claimed Syk-initiated tyrosine-phosphorylation cascade or identify PLCγ2, Vav, and MAPK as its downstream mediators. Page numbers are not available in our copy. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“TREM2+ tumor macrophages co-expressed CD68, CD163, CSF1R, and nuclear MAFB; foamy TREM2+ tumor macrophages also co-expressed MITF, a transcription factor involved in lysosomal biogenesis that marks a regulatory myeloid subset of human placenta (Costa et al., 2017).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Trem2 Is Selectively Expressed in Human Tumor Macrophages
What the sources say
- Supportedcites Costa et al., 2017 source
The Results section reports higher MITF expression in the placental HLA-DRhigh myeloid subset, describes MITF as involved in lysosomal biogenesis, and characterizes that subset as having tolerogenic potential. The citation supports the description of MITF and the placental subset; the sentence does not attribute its tumor-macrophage observations to Costa et al. (LLM, conf=0.90)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“TREM2-signaling pathways, which include not only proliferation and survival, but also metabolism, migration and chemokine production (Peng et al., 2010; Ulland et al., 2017).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > DISCUSSION
What the sources say
- Partly supportedcites Peng et al., 2010 sourceExperimental — accuracy not yet measured
The Results section on SHIP1 and TREM2/DAP12 signaling reports survival signaling, and the Discussion proposes a link between DAP12 signaling and increased proliferation. The paper reports actin reorganization, but does not establish migration; the passages found do not address metabolism or chemokine production. Page numbers are unavailable in our copy. (LLM, conf=0.88)
- Partly supportedcites Ulland et al., 2017 sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) links TREM2 signaling to metabolism, survival, proliferation, and microglial clustering around plaques. Clustering may relate to migration, but the passages do not establish migration as a signaling outcome, and they do not support the claim about chemokine production. (LLM, conf=0.86)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“iNOS2, which has been associated with immunostimulation (Hibbs et al., 1987; Murray et al., 2014; Stuehr and Nathan, 1989), as well as immunosuppression (Shi et al., 2001).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > DISCUSSION
What the sources say
- Not checked — no full text of the sourcecites Hibbs et al., 1987 source
- Could not verifycites Murray et al., 2014 sourceExperimental — accuracy not yet measured
The Background to the problem (p. 4) discusses macrophage activation and arginine metabolism, but does not link iNOS2 to immunostimulation. Searches for iNOS, NOS2, and nitric oxide did not locate a passage in our copy making that association. In the citing sentence, immunosuppression is attributed to Shi et al. (2001), not to this source. (LLM, conf=0.71)
- Not matchedcites Stuehr and Nathan, 1989
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Indeed, all Trem2−/− mice controlled tumor growth as opposed to only a few WT mice (Figures 4D and 4E).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > TREM2 Deficiency Enhances Checkpoint Blockade
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“scRNA-seq revealed that both TREM2 deletion and anti-TREM2 are associated with scant MRC1+ and CX3CR1+ macrophages in the tumor infiltrate, paralleled by expansion of myeloid subsets expressing immunostimulatory molecules that promote improved T cell responses.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Upon depletion of CD8+ T cells (Figure 1E), but not CD4+ T cells (Figure S1C), tumor growth was no longer attenuated, but in fact accelerated in Trem2−/− mice.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > TREM2 Deficiency Delays Growth of Transplanted Tumors and Modifies Tumor-Immune Infiltrate
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Moreover, TREM2 was expressed in all macrophage clusters, although at different levels, while it was absent in DCs and lymphoid cells (Figure S2E).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Lack of TREM2 Impacts Tumor Myeloid and Lymphoid Landscape
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, analysis of T cell cytokine production ex vivo indicated that anti-TREM2 treatment augments IFNγ and TNFα production by intra-tumoral CD8+ and CD4+ T cells, respectively (Figure 5E).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Anti-TREM2 Treatment Is Protective in the Sarcoma Model
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“One of the macrophage subsets that recently immigrated into the tumor, Macs1-t, also declined, while the other one—Macs2-t—expanded, perhaps reflecting changes in the intratumoral differentiation of blood-derived monocytes.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Anti-TREM2 Treatment Reshapes the Intratumoral Macrophages Infiltrate
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Both native and Fc mutated mAb 178 inhibited HDL-induced EGFP expression, indicating that mAb 178 blocks ligand binding to TREM2 (Figure S3B).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Anti-TREM2 Treatment Is Protective in the Sarcoma Model
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“At a later time point (24 days after tumor injection), in parallel with a considerable shrinkage of the tumor volume, anti-TREM2 alone showed a significant impact on the myeloid compartment: while the total number of macrophages was unchanged, the representation of Ly6ClowMHCII− cells, along with subsets expressing CD206, CD63, and CD9, was reduced (Figure S3E).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Anti-TREM2 Treatment Is Protective in the Sarcoma Model
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Following this treatment protocol, only 40% of WT mice rejected the tumor, whereas 100% of Trem2−/− mice did (Figures 4B and 4C).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > TREM2 Deficiency Enhances Checkpoint Blockade
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“scRNA-seq revealed that both TREM2 deletion and anti-TREM2 are associated with scant MRC1+ and CX3CR1+ macrophages in the tumor infiltrate, paralleled by expansion of myeloid subsets expressing immunostimulatory molecules that promote improved T cell responses.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We noticed that CX3CR1-Macs-g, Mrc1-Macs-g, Cycling-Macs-g, and Macs3-g were relatively meagerly represented in Trem2−/− tumors, whereas the Macs1-g cluster predominated (Figures S2B–S2D).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Lack of TREM2 Impacts Tumor Myeloid and Lymphoid Landscape
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“CD8+ T cells were increased in Trem2−/− mice with or without anti-PD-1, as were PD-1+ CD8 T cells, corroborating our initial results (see Figure 1C).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > TREM2 Deficiency Enhances Checkpoint Blockade
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The representation of TREM2+ macrophages was not affected by mAb 178 (Figure S3C), indicating no antibody-mediated depletion, consistent with lack of effector function in the mutated Fc fragment.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Anti-TREM2 Treatment Is Protective in the Sarcoma Model
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Other types of human tumors also showed a correlation between TREM2 and macrophage signature genes, but the association of TREM2 expression with patient overall or relapse-free survival was not significant (data not shown), suggesting that TREM2 impact on tumor-infiltrating macrophages and tumor immune responses might be context specific.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > TREM2 Correlates with Poor Disease Prognosis
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“MCA/1956 grew progressively in WT mice, but was consistently attenuated in Trem2−/− mice (Figures 1A and 1B).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > TREM2 Deficiency Delays Growth of Transplanted Tumors and Modifies Tumor-Immune Infiltrate
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Many macrophage subsets infiltrating MCA/1956 tumors express TREM2.
In the paper
“In atherosclerosis, TREM2+ macrophages are enriched in atherosclerotic lesions and specialize in lipid catabolism (Cochain et al., 2018).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Cochain et al., 2018 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We conclude that anti-TREM2 treatment induces a complex remodeling of the myeloid compartment that drives the appearance of Nos2-Macs-t and a parallel decline of Mrc1-Macs-t, Cycling-Macs-t, and Macs1-t recent immigrants.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Anti-TREM2 Treatment Reshapes the Intratumoral Macrophages Infiltrate
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, TREM2 might be targeted to modify tumor myeloid infiltrates and augment checkpoint immunotherapy.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Yet, treatment of Trem2−/− mice with the anti-TREM2 mAb did not further attenuate tumor growth, demonstrating that anti-TREM2 treatment has no off-target effects.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > RESULTS > Anti-TREM2 Treatment Is Protective in the Sarcoma Model
Load-bearingStrength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Although TREM2 is expressed on the cell surface, it is cleaved from the cell surface by metalloproteases and released as soluble TREM2 (sTREM2) (Ulland and Colonna, 2018).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Ulland and Colonna, 2018 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“In the skin, TREM2+ dermal macrophages secrete oncostatin M, which inhibits hair growth by maintaining hair follicle stem cells in a quiescent state (Wang et al., 2019).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Wang et al., 2019 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“TREM2 has been extensively studied in microglia for its capacity to sustain microglial responses to neurodegenerative pathologies such as Alzheimer’s disease (Ulland and Colonna, 2018).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Ulland and Colonna, 2018 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The anti-TREM2 treatment presented here provides a novel therapeutic approach that broadens the armamentarium for myeloid cell targeting in tumors.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > DISCUSSION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“During lung acute viral infection, TREM2+ macrophages release sTREM2, which inhibits apoptosis of macrophages, causing a feed-forward expansion of lung macrophages that converts acute infection into a chronic inflammatory disease (Wu et al., 2015).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > INTRODUCTION
What the sources say
- Not matchedcites Wu et al., 2015
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This study demonstrates that constitutive lack of TREM2 or anti-TREM2 treatment curbs tumor growth and leads to complete tumor regression when associated with suboptimal PD-1 immunotherapy.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > DISCUSSION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Cells identified as doublets or mutliplets based on gene expression signatures, when more than one cell population-specific marker gene was highly expressed in one cell, were filtered out.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > STAR★METHODS > QUANTIFICATION AND STATISTICAL ANALYSIS
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Cells with mitochondrial content greater than 12.5% and with less than 1100 genes were removed.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > STAR★METHODS > QUANTIFICATION AND STATISTICAL ANALYSIS
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Mice from different genotypes were cohoused from birth and separated during the experiment (the day of tumor injection).”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > STAR★METHODS > EXPERIMENTAL MODEL AND SUBJECT DETAILS
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“our extensive pathology study of human tumors suggests that TREM2 may be a particularly attractive therapeutic target”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > DISCUSSION
Tests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All animals were backcrossed until at least > 98% C57BL/6J confirmed by genotype wide microsatellite typing.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > STAR★METHODS > EXPERIMENTAL MODEL AND SUBJECT DETAILS
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“Mice within experiments were age and sex matched.”
§ TREM2 Modulation Remodels the Tumor Myeloid Landscape, Enhancing Anti-PD-1 Immunotherapy > STAR★METHODS > EXPERIMENTAL MODEL AND SUBJECT DETAILS
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
Many macrophage subsets infiltrating MCA/1956 tumors express TREM2.
“These tumors have recently been shown to be infiltrated by a variety of macrophage subsets (Gubin et al., 2018), many of which express TREM2 (unpublished data).”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In our previous study, a mouse TREM2 blocking antibody, with mutations in the Fc domain to prevent its recognition by the Fc receptor and complement, was developed and shown to block the binding of TREM2 and its high-avidity ligands38.”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [38]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“and are known to be associated with failure of CPI targeting the PD-1/PD-L1 axis.80,81”
From Cystatin C is glucocorticoid responsive, directs recruitment of Trem2+ macrophages, and predicts failure of cancer immunotherapy (2023) · cites this paper as [81]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“we propose a model in which CyC is associated with recruitment of immunosuppressive Trem2+ macrophages,80,81 which in turn promote failure of cancer immunotherapy.”
From Cystatin C is glucocorticoid responsive, directs recruitment of Trem2+ macrophages, and predicts failure of cancer immunotherapy (2023) · cites this paper as [81]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“High-confidence Trem2+ monocytes were identified by expression of known TREM2+ monocyte markers (TREM2, APOE, CSF1R81,89), identified by gene-weighted density estimation implemented in the Nebulosa package for R.78”
From Cystatin C is glucocorticoid responsive, directs recruitment of Trem2+ macrophages, and predicts failure of cancer immunotherapy (2023) · cites this paper as [81]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“This antibody is particularly useful because it can specifically demonstrate the effect of receptor TREM2 blockade without the confounding activity of antibody-dependent cellular cytotoxicity or antibody-dependent phagocytosis in vivo.”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [38]
The cited source says what the claim attributes to it.
In the citing paper
“All blocking experiments were conducted with the anti-TREM2 mAb 178, which has been previously shown to block TREM2 function in vitro and in vivo (27–31).”
From Acute TREM2 inhibition depletes MAFB-high microglia and hinders remyelination (2025) · cites this paper as [27]
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Self-check results appear here once an independent check has confirmed them.
Cited works that were retracted
Works this paper cites that were later retracted, from the retraction notices publishers deposit. Major when the notice came out before this paper was published.
Cites a retracted work: 10.1172/jci98769
InfoThe cited work was retracted on 2022-03-15 (notice 10.1172/jci159825), not before this paper was published (2020-08).
Cited work 10.1172/jci98769 · retracted 2022-03-15 · notice 10.1172/jci159825 · this paper published 2020-08
“Although the MCA/1956 sarcoma grows progressively in immunocompetent hosts, it retains sufficient immunogenicity to be effectively controlled by checkpoint immunotherapy with anti-PD-1 (Li et al., 2018).”
Citations
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“Although the MCA/1956 sarcoma grows progressively in immunocompetent hosts, it retains sufficient immunogenicity to be effectively controlled by checkpoint immunotherapy with anti-PD-1 (Li et al., 2018).”
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“Since these tumors were developed in immunocompetent WT mice, their immunogenic profiles were edited by the immune system, and hence, they grow unopposed when transplanted into naive syngeneic WT hosts (Alspach et al., 2019; Schreiber et al., 2011; Shankaran et al., 2001).”
Self-citationMacrophage activation and polarization: nomenclature and experimental guidelines
Murray, P. J., Allen, J. E., Biswas, S. K., Fisher, E. A., Gilroy, D. W., Goerdt, S., Gordon, S., Hamilton, J. A., Ivashkiv, L. B., Lawrence, T., et al. (2014) · Immunity · doi:10.1016/j.immuni.2014.06.008 · Cited by 6,337 · cited 1×
“Moreover, the macrophage subset inflated in anti-TREM2-treated mice expressed iNOS2, which has been associated with immunostimulation (Hibbs et al., 1987; Murray et al., 2014; Stuehr and Nathan, 1989), as well as immunosuppression (Shi et al.”
Freeman, G. J., Long, A. J., Iwai, Y., Bourque, K., Chernova, T., Nishimura, H., Fitz, L. J., Malenkovich, N., Okazaki, T., Byrne, M. C., et al. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.192.7.1027 · Cited by 5,294 · cited 1×
“lymphocyte associated antigen-4 (CTLA-4) and programmed death-1 (PD-1) (Freeman et al., 2000; Leach et al., 1996).”
The future of immune checkpoint therapy
Sharma, P., & Allison, J. P. (2015) · Science · doi:10.1126/science.aaa8172 · Cited by 4,878 · cited 1×
“mAb inhibiting CTLA-4 or PD-1 have been extensively shown to unleash T cell effector functions to control tumors in both mice and some cancer patients (Sharma and Allison, 2015; Topalian et al., 2015).”
Immune Checkpoint Blockade: A Common Denominator Approach to Cancer Therapy
Topalian, S. L., Drake, C. G., & Pardoll, D. M. (2015) · Cancer Cell · doi:10.1016/j.ccell.2015.03.001 · Cited by 4,229 · cited 1×
“mAb inhibiting CTLA-4 or PD-1 have been extensively shown to unleash T cell effector functions to control tumors in both mice and some cancer patients (Sharma and Allison, 2015; Topalian et al., 2015).”
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Items 401–500 of 657
Determinants, mechanisms, and functional outcomes of myeloid cell diversity in cancer
Caronni, N., Montaldo, E., Mezzanzanica, L., Cilenti, F., Genua, M., & Ostuni, R. (2021) · Immunological Reviews · doi:10.1111/imr.12944 · Cited by 6
Tao, K., Chen, C., Xu, G., et al. (2024) · Translational Cancer Research · doi:10.21037/tcr-23-2328 · Cited by 6
“Preclinical studies have reported that anti-VEGF/VEGFR-2 alters the invasion of a series of tumor-type lymphocytes or macrophages, and its combined use with immunotherapy enhances the antitumor effect (32-34).”
Pierro, E. W., Cottam, M. A., An, H., Lehmann, B. D., Pietenpol, J. A., Wellen, K. E., Makowski, L., Rathmell, J. C., Fingleton, B., & Hasty, A. H. (2025) · Cancer Research · doi:10.1158/0008-5472.can-24-3511 · Cited by 8
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Mu, X.-Y., Chen, S.-B., Yang, S.-Y., Wang, W., Zhou, H., Wang, Y., Chen, X.-Y., Peng, X., & Li, W. (2025) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2025.143163 · Cited by 8
Li, B., Jiang, Y.-Y., Li, X., Yu, M., Meng, Q., Wang, D., Zang, J.-M., & Xu, F. (2025) · BMC Complementary Medicine and Therapies · doi:10.1186/s12906-025-05020-8 · Cited by 6
“Thus, targeted therapy with anti-TREM2 antibodies can induce immune responses, inhibit tumor progression, and enhance ICB efficacy [15], making TREM2 a potential target for cancer immunotherapy.”
InfluentialTREM2 and LAG-3 in cancer and Alzheimer’s disease immunotherapy
Yuan, S., Fuchs, N. S., Abdel‐Rahman, S. A., Kaur, B., & Gabr, M. T. (2025) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2025.06.010 · Cited by 6
Pervizou, D., Chiara, J. D., Spinelli, L., NESTOR-MARTIN, M., Chasson, L., LEN-TAYON, K., Yanushko, D., FIORE, F., Bajénoff, M., Malissen, B., et al. (2025) · OncoImmunology · doi:10.1080/2162402x.2025.2562220 · Cited by 6
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Tan, Y., Yang, T., Jiang, S., Li, S., Cai, L., Wang, Y., Guo, Z., & Wang, X. M. (2026) · Journal of Inorganic Biochemistry · doi:10.1016/j.jinorgbio.2026.113212 · Cited by 7
Zhao, Q., Huang, R., Wang, C., Hu, J., Nie, R. C., Jian, R., Wang, Y., Wang, D., Liang, C., Chen, Y., et al. (2026) · Cancer Cell · doi:10.1016/j.ccell.2026.01.015 · Cited by 10
Self-citationThe emerging role of triggering receptor expressed on myeloid cell-2 in malignant tumor
Wang, Y., Chu, Y., Cao, F., Chen, Z., Xu, H., Wang, S., & Ma, J. (2023) · Central European Journal of Immunology · doi:10.5114/ceji.2022.124387 · Cited by 7
“TAMs are believed to be one of the most important populations infiltrated in TME, related to poor prognosis and low response to immunotherapy [56].”
BackgroundInfluentialGao, H., Yang, Z., Sun, H., Zhang, Y., Wang, Z., Liu, W., Wen, H., Qu, C., & Wang, X. (2023) · PubMed Central · Cited by 6
Systematic analysis of TREM2 and its carcinogenesis in pancreatic cancer
Zheng, W., Yu, W., Hua, R., He, J., Wu, N., Tian, S., Huang, W., & Qin, L. (2024) · Translational Cancer Research · doi:10.21037/tcr-24-201 · Cited by 6
“TREM2 expression is restricted within most normal tissue, whereas approximately 75% of cancer types have been shown to express TREM2 (11).”
TREM2 Is Associated with Advanced Stages and Inferior Prognosis in Oral Squamous Cell Carcinoma
Struckmeier, A., Radermacher, A., Fehrenz, M., Alansary, D., Wartenberg, P., Wagner, M., Scheller, A., Heß, J., Moratin, J., Freudlsperger, C., et al. (2022) · Cancers · doi:10.3390/cancers14194635 · Cited by 6
“provided evidence that triggering receptor expressed on myeloid cells 2 (TREM2) is a potential target in cancer therapy [8].”
BackgroundCystatin C is a glucocorticoid response gene predictive of cancer immunotherapy failurePreprint
Kleeman, S. O., Ferrer, M., Demestichas, B., Bankier, S., Lee, H., Heywood, T., Ruusalepp, A., Bjorkegren, J. L. M., Walker, B., Meyer, H. V., et al. (2021) · medRxiv · doi:10.1101/2021.08.17.21261668 · Cited by 4
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Macrophage crosstalk and therapies: Between tumor cells and immune cells
Fan, C.-Y., Zheng, J.-S., Hong, L., & Ling, Z. (2024) · International Immunopharmacology · doi:10.1016/j.intimp.2024.113037 · Cited by 5
Qin, Z., Bian, X., & Shi, Y. (2024) · Clinical and Translational Medicine · doi:10.1002/ctm2.70013 · Cited by 5
“13,14 A comprehensive investigation of TAM heterogenicity and the contribution of distinct TAM subpopulations to each specific tumour type and stage is a prerequisite for the rational design of macrophage-centred therapies.”
BackgroundSoluble TREM2 drives triple-negative breast cancer progression via activation of the AKT pathway
Yin, P., Jiang, Y., Ji, X., Lin, X., Su, Z., & Tian, Y. (2024) · International Immunopharmacology · doi:10.1016/j.intimp.2024.113750 · Cited by 5
Ding, X.-Y., Wu, Q., Du, Y., Ji, M.-M., Yang, H., Hu, Q.-S., & Ye, Y.-Q. (2025) · Small Methods · doi:10.1002/smtd.202401192 · Cited by 7
Shen, R., Cao, W., Wang, L., Sheng, L., Zhang, Y., Wu, W., Xu, P., Cheng, S., Liu, M., Dong, Y., et al. (2025) · Clinical and Translational Medicine · doi:10.1002/ctm2.70310 · Cited by 5
“25 The combination of anti-TREM2 treatment with immunotherapy promotes expansion of immunostimulatory myeloid subsets, enhancing the anti-tumour activity of immunotherapy such as ICIs or CAR T-cell therapy.”
The Role of TREM2 After Stroke: From Mechanisms to Therapeutic Potential
Zhou, T., Chen, A., Sun, Y., Huang, B., Xu, Y., & He, Q. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-05622-w · Cited by 6
“Antago-nizing TREM2 signaling or depleting TREM2-expressing myeloid cells may represent a regulatory direction for cancer treatment [55, 56, 103, 104].”
Xu, Y., Shen, H., Shang, D., & Zhu, C. (2026) · Frontiers in Oncology · doi:10.3389/fonc.2025.1665239 · Cited by 10
“In transplantable chemically induced sarcoma and genetically engineered sarcoma models expressing immunodominant antigens, CD8 + T cells recognized epitopes corresponding to neoantigens in rejected tumors (225, 226).”
Li, X., Wang, Z., Mao, S., Zhao, Y., Ye, J., Liang, B., Peng, J., Xie, X., Pan, J., Xiao, C., et al. (2026) · iScience · doi:10.1016/j.isci.2025.114607 · Cited by 6
Pathophysiological roles of monocytes and macrophages in cancer
Ji, L., Li, J., Hsu, T.-W., & Li, M. O. (2026) · Nature reviews. Immunology · doi:10.1038/s41577-026-01296-0 · Cited by 8
“…clearance 33 , improves neoantigen vaccine efficacy 175 and synergizes with anti-PD1 therapy to trigger CD8 + T cell-mediated immunity with enrichment of ‘IFNγ signalling/CXCL9’-like macrophages 176,177 — effects that may partly reflect shifts in intestinal macrophages and the microbiota 178 .”
Wang, P.-X., Zhong, Y.-C., Zheng, W.-J., Xian, J., Song, F., Xu, J., Sun, Y., Cheng, J.-W., Feng, H.-Y., Jiang, X., et al. (2026) · Cancer Letters · doi:10.1016/j.canlet.2026.218657 · Cited by 5
TREM2+ macrophages are guardians of the heart
Nicolás-Ávila, J. Á., & Hidalgo, A. (2023) · Nature Metabolism · doi:10.1038/s42255-022-00712-8 · Cited by 5
Suryadevara, N., Kose, N., Bangaru, S., Binshtein, E., Munt, J. E., Martinez, D. R., Schäfer, A., Myers, L., Scobey, T., Carnahan, R. H., et al. (2024) · Journal of Clinical Investigation · doi:10.1172/jci178880 · Cited by 6
“Similar to mAb C1717, other mAbs, such as S2M24 (19), DH1052 (29), and polyclonal Fabs from donor COV57 (49), also were identified in individuals following SARS-CoV-2 infection.”
TREM2 as a Therapeutic Target in Atherosclerosis
Xu, S., Yang, B., Yu, W., Gao, Y., Cai, H., & Wang, Z. (2025) · Cell Biology International · doi:10.1002/cbin.12279 · Cited by 7
“The high TREM2 expression level is associated with lower tumor progression (Molgora et al. 2020b) and survival in patients with gastric cancer, glioma (Deczkowska, Weiner, and Amit 2020), and hepato-cellular carcinoma (Perugorria et al. 2019).”
Insights from a Computational-Based Approach for Analyzing Autophagy Genes across Human Cancers
Carrasco, A. G. M., Giovanini, G., Ramos, A. F., Chammas, R. J., & Bustos, S. O. (2023) · Genes · doi:10.3390/genes14081550 · Cited by 5
“TREM2 deficiency delays tumor growth in mice [26].”
BackgroundImmune checkpoints targeting dendritic cells for antibody-based modulation in cancer
Lei, X., Wang, Y., Broens, C., Borst, J. G., & Xiao, Y. (2023) · International review of cytology · doi:10.1016/bs.ircmb.2023.07.006 · Cited by 5
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Role of Yoga as Adjunctive Therapy for Migraines: A Narrative Review of the Literature
Kachhadia, M. P., Khalil, Z. M., Shah, S. C., Fawad, M., Sajjad, H., Yadav, K. P., Kanthala, N. R., Patel, T., Egbujo, U. C., & Basant, K. (2023) · Cureus · doi:10.7759/cureus.48434 · Cited by 5
“Table 2 summarizes some of the benefits of yoga versus medications in different aspects of migraine headaches [49-51].”
BackgroundLi, H., Xu, D., Cai, W., Liu, J., Bing, Z., & Zhang, Q. (2024) · Advanced Healthcare Materials · doi:10.1002/adhm.202403096 · Cited by 5
A review of common immunotherapy and nano immunotherapy for acute myeloid leukemia
Wang, Y., Yang, X., Liu, Y., & Li, Y. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1505247 · Cited by 5
Zhao, Z., Wang, Z., Wu, Y., Liao, D., & Zhao, B. (2022) · Molecular Immunology · doi:10.1016/j.molimm.2022.02.012 · Cited by 6
A Pan-Cancer Census of Dominant Tumor Immune ArchetypesPreprint
Combes, A. J., Samad, B., Tsui, J., Chew, N. W., Yan, P., Reeder, G. C., Kushnoor, D., Shen, A., Davidson, B., Barczac, A. J., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.04.26.441344 · Cited by 5
“…the genes identified have been previously associated to their respective MPC subsets such as VCAN, TREM2, CD1C, CLEC9A and LAMP5 in monocytes, macrophages, cDC2, cDC1 and pDCs, respectively (Binnewies et al., 2018; Cheng et al., 2021; Combes et al., 2017; Molgora et al., 2020; Sancho et al., 2009).”
BackgroundPeters, J. M., Gideon, H. P., Hughes, T. K., Gunnarsson, C., Maiello, P. A., Mugahid, D., Nyquist, S. K., Bromley, J. D., Blainey, P. C., Junecko, B. A. F., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.05.24.595747 · Cited by 4
“Loss of TREM2 expression or activity has been shown to reduce tumor burden in several models of lung cancer 84,98 .”
BackgroundZou, X., Wang, Y., Luan, M., & Zhang, Y. (2025) · Frontiers in Pharmacology · doi:10.3389/fphar.2025.1605162 · Cited by 5
Distinct TAM subset with cross-dressing capability determines the bifurcation of tumor immunity
Shimizu, K., Sanpei, A., Nakazato, H., Shinga, J., Ueda, S., Liu, Y., Iyoda, T., Yamasaki, S., Nakabayashi, J., & Fujii, S. (2025) · Cell Reports · doi:10.1016/j.celrep.2025.115800 · Cited by 5
Daytime SHP2 inhibitor dosing, when immune cell numbers are elevated, shrinks neurofibromas
Ahmari, N., Choi, K., Wu, J., Rizvi, T. A., Jackson, M., Kershner, L. J., Kim, M., Zhang, X., Dombi, E., Shern, J. F., et al. (2025) · Life Science Alliance · doi:10.26508/lsa.202503359 · Cited by 5
“Mice treated with vehicle or with weekly anti-PD1, a checkpoint inhibitor used to activate tumor T cells (Topalian et al, 2016; Molgora et al, 2020), showed growing tumors, whereas SHP2 inhibitor shrank most tumors.”
CARD9-dependent macrophage plasticity regulates effective fungal clearance
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CAR-T triggers TAM reeducation and adaptive anti-tumor response via TREM2 deficiency or CD40 agonist
Liu, T., Gao, H., Xi, Z., Yu, T., Gu, Y., Mai, H., Yuan, H., Liu, Y., Liu, H., Zhang, Q., et al. (2026) · Cell Reports Medicine · doi:10.1016/j.xcrm.2025.102539 · Cited by 5
Leveraging macrophage plasticity for precision-targeted tumor immunotherapy
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Reprogramming T cell-myeloid crosstalk overcomes immune resistance in colorectal cancer
Mestrallet, G., Brown, M., Vaninov, N., Cho, N. W., Velazquez, L. G., Ananthanarayanan, A., Spitzer, M. H., Vabret, N., Bozkus, C. C., Samstein, R. M., et al. (2026) · Cell Reports Medicine · doi:10.1016/j.xcrm.2026.102786 · Cited by 4
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The tumour microenvironment of pilocytic astrocytoma evolves over time via enrichment for microglia
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“However, in other malignancies including glioma, it is noted as a negative prognostic marker and is thought to modulate anti-tumour immune responses through immunosuppressive activity, further supporting the hypothesis that these represent microglia co-opted into a supportive role [31, 41, 43, 56].”
Characterizing macrophage diversity in colorectal malignancies through single-cell genomics
Zhao, T., Luo, Y., Sun, Y., & Wei, Z. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1526668 · Cited by 7
“The triggering receptor expressed on myeloid cell 2 (TREM2) represents a potential therapeutic target for modulating immunosuppressive TAMs (159).”
Barrio‐Alonso, C., Nieto‐Valle, A., Barandalla-Revilla, L., Avilés-Izquierdo, J. A., Parra‐Blanco, V., Sánchez‐Mateos, P., & Samaniego, R. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1587545 · Cited by 4
Luo, B., Luo, Y., Chen, S., Yang, T., Liu, B., Liao, X., Zheng, X., Tian, T., Liu, J., Zhan, Q., et al. (2025) · Advanced Science · doi:10.1002/advs.202413256 · Cited by 4
Liu, J., Shi, Z., Li, Y., Ma, J., Yao, J., Yuan, Z., Wang, Y., Yang, C., Li, X., Xing, N., et al. (2025) · EBioMedicine · doi:10.1016/j.ebiom.2025.105801 · Cited by 5
Metabolites in the extracellular tumor microenvironment and the shaping of macrophage function
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Who is who within the universe of TREM-like transcripts (TREML)?
Ertel, M. V., da Silva, A. B. A., de Sousa, D. F., dos Santos, C. J., da Silva, T. M., Silva‐Sales, M., Matos, A. D. O., & Sales‐Campos, H. (2024) · Life Sciences · doi:10.1016/j.lfs.2024.122696 · Cited by 4
Bibliometric Analysis of TREM2 (2001-2022): Trends, Hotspots and Prospects in Human Disease
Qian, M., Zhong, J., Lu, Z., Zhang, W., Weng, M., Zhang, K., & Jin, Y. (2024) · International Journal of Medical Sciences · doi:10.7150/ijms.96851 · Cited by 4
“In patients with non-small cell lung cancer, TREM2 acts as a negative immunoregulatory molecule, and its expression is positively correlated with tumor progression [66].”
BackgroundPeng, K., Zhang, X., Li, Z.-L., Wang, Y.-C., Sun, H.-W., Zhao, W., Pan, J., Zhang, X.-Y., Wu, X., Yu, X.-R., et al. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1493735 · Cited by 4
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Ramos, R. N., Missolo-Koussou, Y., Gerber-Ferder, Y., Bromley, C. P., Bugatti, M., Núñez, N. G., Tosello, J., Richer, W., Denizeau, J., Sedlik, C., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.04.12.439412 · Cited by 4
“TREM2+ TAMs have been shown to infiltrate tumor nest across cancers (Molgora et al., 2020).”
BackgroundResultInfluentialSelf-citationCottam, M. A., Caslin, H. L., Winn, N. C., & Hasty, A. H. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.08.20.455954 · Cited by 4
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Sopa: a technology-invariant pipeline for analyses of image-based spatial-omicsPreprint
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Obesity and Cancer: From Systemic Metabolic Reprogramming to Immunotherapy Paradox
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Myeloid diversity in tumors: Shaped by genes, location, and time
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Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition
Yu, H., Zhao, M., Li, Q., & Zhang, Y. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1787094 · Cited by 4
“TREM2 + TAMs exhibit a distinct lipid-metabolic program, with increased fatty acid uptake, lipid droplet accumulation, and SPP1 expression, promoting immunosuppressive and pro-invasive phenotypes (176 – 178).”
Harnessing myeloid cell plasticity for cancer therapy
Sanseviero, E., Barry, S. T., & Gabrilovich, D. I. (2026) · Nature Cancer · doi:10.1038/s43018-026-01159-6 · Cited by 5
“Genetic deletion of TREM2 reduced tumor growth and improved the response to anti-PD-1 therapy 73 .”
Talkhoncheh, M. S., Sjölund, J., Bolívar, P., Kurzejamska, E., Cordero, E., Pagès, T. V., Larsson, S., Lehn, S., Frimannsson, G., Ingesson, V., et al. (2025) · Journal of Clinical Investigation · doi:10.1172/jci183086 · Cited by 4
“Notably, TREM2 also denotes immunosuppressive (and M2-like) TAMs with a putative monocytic origin (49, 50).”
Sun, J., Zhou, S., Sun, Y., & Zeng, Y. (2025) · Frontiers in Medicine · doi:10.3389/fmed.2025.1541104 · Cited by 4
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“32,54,55 Lipid metabolism is enriched in this population, 56 a functional category of the genes differentially expressed in 3D macrophages (Figure 3b).”
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“Recently, studies have shown that TREM1 signaling compromises TIME in various cancer types [58–61].”
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zhao, M., Jankovic, D. L., Link, V. M., Souza, C. O. S., Hornick, K. M., Oyesola, O. O., Belkaid, Y., Lack, J., & Loke, P. (2025) · Nature Communications · doi:10.1038/s41467-025-56379-8 · Cited by 5
“1h), whereas Trem2 , which is important in Alzheimer ’ s disease and cancer 19,20 , is an IL-4 induced gene speci fi c for BL/6 macrophages (Fig.”
Cavity macrophages stop anti-tumor T cells
Rodrı́guez, P. C., & Ruffell, B. (2021) · Cancer Cell · doi:10.1016/j.ccell.2021.06.007 · Cited by 3
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“Fc domain enhanced anti-TREM2 monoclonal antibody was shown to impair tumor growth in mice by enhancing anti-tumor CD8 T cell responses and altering the balance between immunosuppressive and immunostimulatory macrophages 134 .”
Mestrallet, G., Brown, M., Vaninov, N., Cho, N. W., Velazquez, L. G., Ananthanarayanan, A., Spitzer, M. H., Vabret, N., Bozkus, C. C., Samstein, R. M., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.02.12.637954 · Cited by 3
Segal, J. E., Cronk, J. C., Ball, B., Forbes, G. E., Jackett, K. N., Li, K. P., Osorno, A. M., Montalvan, E. S. A., Browne, A., Lake, J. A., et al. (2025) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a041609 · Cited by 3
Cancer cell phagocytosis induces an anti-inflammatory gene regulatory program in macrophagesPreprint
Zhang, C. R., Xiong, L., Gu, M., Yeh, C. Y., Jerby‐Arnon, L., Kundaje, A. B., Greenleaf, W. J., & Bassik, M. C. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.08.18.670953 · Cited by 3
Mouse models for cancer research – current state and the perspective
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“A study targeted at the efficacy of anti-PD1 treatment on myeloid tumors demonstrated the impact of Trem2 receptors on the TME via knock-out Trem2 mice [122].”
BackgroundLee, K., Kim, S., Zhao, J., & Neo, S. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1631258 · Cited by 2
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“38–40 Notably, M ϕ s in the TME of NR patients exhibited higher expression levels of checkpoints than R patients (figure 5d), suggesting stronger immunosuppressive functions.”
Membrane IL-18 identifies a human macrophage subset with distinct proteomic and functional traits
Vitale, C., Petretto, A., Cortese, K., Carta, S., Dondero, A., Lavarello, C., Cangelosi, D., Morini, M., Bellora, F., Arnaldi, P., et al. (2025) · OncoImmunology · doi:10.1080/2162402x.2025.2571774 · Cited by 2
“12,18,19 In contrast, FOLR2+ macrophages are tissue-resident macrophages colonizing healthy tissues, which in tumors interact with tumor-infiltrating CD8+ T promoting their expansion and activation.”
Self-citationFeng, H., Liang, S., Wang, D., Xu, S., & Qin, G. (2025) · Clinical and Experimental Medicine · doi:10.1007/s10238-025-01920-8 · Cited by 3
“For instance, several studies have demonstrated that TAMs expressing TREM2 exhibit impaired phagocytic function and create an immunosuppressive niche, despite potentially expressing certain inflammatory genes [44, 45].”
Barizza, A., Vassallo, S., Masatti, L., et al. (2025) · Journal for ImmunoTherapy of Cancer · doi:10.1136/jitc-2025-013249 · Cited by 2
“36 Although tumor-infiltrating T cells were present at a low frequency, their CD4 + and CD8 + proportions were similar between genotypes (online supplemental figure 3F).”
Self-citationRaja, M. R. K., Gupta, G., Atkinson, G., Kathrein, K. L., Armstrong, A. R., Gower, R. M., Roninson, I. B., Broude, E. V., Chen, M., Ji, H., et al. (2026) · npj Breast Cancer · doi:10.1038/s41523-026-00890-8 · Cited by 6
“These results are in line with several previous reports showing that CX3CR1 + TAMs commonly display high phagocytic but immune suppressive activities 26,38,39 .”
Xiong, C., Ning, H., Wang, X., Xie, Y., Liu, Z., Hu, D., & Gao, X. (2026) · Journal of Advanced Research · doi:10.1016/j.jare.2026.01.048 · Cited by 2
Clinical optimization of bexmarilimab as a myeloid checkpoint therapy
Karthikeyan, M., Mickos, J., & Hollmén, M. (2025) · Immunotherapy · doi:10.1080/1750743x.2026.2617035 · Cited by 2
“Similar to T-cell check-points, these pathways, including SIRPα/CD47 [6], LILRBs [7], TIM-3 [8], VISTA [9], TREM2 [10], and MARCO [11], maintain myeloid cells in a suppressive or tolerogenic state, limiting phagocytosis, antigen presentation, and support for effector T-cell responses.”
Xing, Y., Zhong, R., Li, Q., Duan, X., Xu, M., Yu, M., Liu, C., He, J., Sun, Y., Wang, Y., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-69060-5 · Cited by 2
“TREM2 is predominantly expressed on tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) 65 , and its inhibition has been shown to enhance checkpoint immunotherapy ef fi cacy across multiple cancers, including sarcoma, colorectal, and breast cancers 15 .”
InfluentialLi, J., Liu, M., Peng, Y., & Wu, R. (2026) · Arthritis Research & Therapy · doi:10.1186/s13075-026-03764-3 · Cited by 2
“TREM2 + macrophages have recently been identified as a specialized subset in various tissue contexts, including tumor microenvironments and neurodegenerative diseases, where they adopt a lipid-associated, pro-survival phenotype [28, 29].”
Metadata
- Authors
- Molgora, M., Esaulova, E., Vermi, W., Hou, J., Chen, Y., Luo, J., Brioschi, S., Bugatti, M., Omodei, A. S., Ricci, B., Fronick, C., Panda, S. K., Takeuchi, Y., Gubin, M. M., Faccio, R., Cella, M., Gilfillan, S., Unanue, E. R., Artyomov, M. N., Schreiber, R. D., & Colonna, M.
- Affiliations
- Washington University in St. Louis (US)
- University of Brescia (IT)
- The University of Texas MD Anderson Cancer Center (US)
- Corresponding author
- Colonna, Marco
- ORCID
- Molgora, Martina
- Esaulova, Ekaterina
- Vermi, William
- Hou, Jinchao
- Chen, Yun
- Luo, Jingqin
- Brioschi, Simone
- Bugatti, Mattia
- Omodei, Andrea Salvatore
- Ricci, Biancamaria
- Fronick, Catrina
- Takeuchi, Yoshiko
- Gubin, Matthew M.
- Faccio, Roberta
- Cella, Marina
- Gilfillan, Susan
- Unanue, Emil R.
- Artyomov, Maxim N.
- Schreiber, Robert D.
- Colonna, Marco
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2020-08
- Volume
- 182
- Issue
- 4
- Pages
- 886-900.e17
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC7485282
- OpenAlex
- W3048665145
- Semantic Scholar
- f3e033b1cb47f2b00fc56e9c646a9bcdde754590
- Cited by
- 656
- References
- 65
- Citations by year
- 2026: 117 · 2025: 124 · 2024: 127 · 2023: 116 · 2022: 97 · 2021: 63 · 2020: 11
- FWCI
- 23.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion)
- Institutional Research Information System (Università degli Studi di Brescia) (submittedVersion)
- Funders
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- TREM2, tumor-infiltrating macrophages, anti-PD-1 therapy, cancer immunotherapy, TREM2 knockout mice, CX3CR1+ macrophages, immunosuppressive myeloid cells, T cell response
- MeSH terms
- CX3C Chemokine Receptor 1, Animals, Antibodies, Monoclonal, Disease Models, Animal, Humans, Immunotherapy, Membrane Glycoproteins, Methylcholanthrene, Mice, Inbred C57BL, Neoplasms, Prognosis, Receptors, Immunologic, Lymphocytes, Tumor-Infiltrating, Mice, Knockout, Cell Line, Tumor, Mice, Tumor Microenvironment, Programmed Cell Death 1 Receptor
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