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Lipid-Associated Macrophages Control Metabolic Homeostasis in a Trem2-Dependent Manner
Open accessAbstract
Immune cells residing in white adipose tissue have been highlighted as important factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that drive adipose tissue immune cell remodeling during obesity remain largely unknown. Using index and transcriptional single-cell sorting, we comprehensively map all adipose tissue immune populations in both mice and humans during obesity. We describe a novel and conserved Trem2+ lipid-associated macrophage (LAM) subset and identify markers, spatial localization, origin, and functional pathways associated with these cells. Genetic ablation of Trem2 in mice globally inhibits the downstream molecular LAM program, leading to adipocyte hypertrophy as well as systemic hypercholesterolemia, body fat accumulation, and glucose intolerance. These findings identify Trem2 signaling as a major pathway by which macrophages respond to loss of tissue-level lipid homeostasis, highlighting Trem2 as a key sensor of metabolic pathologies across multiple tissues and a potential therapeutic target in metabolic diseases.
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“MASH is associated with the emergence of lipid-associated macrophages (LAM) that highly express Trem2 along with Cd9, Gpnmb, and Spp1 (3–5)”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [4]
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
“While the majority of murine studies to date have suggested a role for LAMs/LAM-like KCs in tissue repair, contributing to dead cell and lipid clearance, thus reducing lipotoxic stress, and preventing uncontrolled inflammation (36, 108, 122–126)”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [126]
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
“TREM2 ligands include a variety of molecules, such as bacterial wall products, Aβ oligomers, lipoproteins, and anionic lipids, such as phospholipids and sphingolipids29,32–35”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [33]
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In the citing paper
“Notably, these included the lysosomal enzymes ASAH1, LIPA, CTSA, CTSG, CTSZ, PLA2G15 and PPT1, enzymes part of the Coordinated Lysosomal Expression and Regulation network60, as well as PLA2G7, previously associated with atherosclerotic plaques61 and with the LAM48 and MIMS-foamy microglial states11.”
From Foamy microglia link oxylipins to disease progression in multiple sclerosis (2026) · cites this paper as [48]
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In the citing paper
“The foamy, GPNMB+ microglial phenotype in MS lesions bears striking transcriptional similarity to LAMs in obesity, amyloid-responsive microglia in Alzheimer’s disease and foam cells in atherosclerosis18,46,48,50,51.”
From Foamy microglia link oxylipins to disease progression in multiple sclerosis (2026) · cites this paper as [48]
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“The disease-associated phenotype of microglia seems to be shared by aging, as well as neurological and non-neurological diseases with different etiology, e.g. AD and amyotrophic lateral sclerosis (Holtman et al., 2015; Keren-Shaul et al., 2017), atherosclerosis and obesity, characterized by lipid overload (Jaitin et al., 2019; Martinet et al., 2019).”
From Alzheimer's-associated PU.1 expression levels regulate microglial inflammatory response (2021) · cites this paper as Jaitin et al., 2019
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“There was considerable overlap between the Micro_D profile and previously reported microglial states, such as the MIMS-foamy state reported in ref. 11, amyloid-associated microglia in Alzheimer’s disease43,46,47 and lipid-associated macrophages (LAMs) in obesity48 (Extended Data Fig. 8).”
From Foamy microglia link oxylipins to disease progression in multiple sclerosis (2026) · cites this paper as [48]
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“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).”
From TREM2 Modulation Remodels the Tumor Myeloid Landscape Enhancing Anti-PD-1 Immunotherapy (2020) · cites this paper as Jaitin et al., 2019
The cited source says what the claim attributes to it.
In the citing paper
“lipid-associated macrophages have recently been identified in mouse and human adipose tissue, where TREM2 expression was found to regulate lipid homeostasis [57].”
From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [57]
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“These cells had a similar transcriptional profile to DAM [57]”
From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [57]
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“although the mouse DAM transcriptome profile may not be fully present in AD brain, as human microglia show a distinct AD-related gene signature (Jaitin et al., 2019; Mathys et al., 2019).”
From Alzheimer's-associated PU.1 expression levels regulate microglial inflammatory response (2021) · cites this paper as Jaitin et al., 2019
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“However, in experimental liver fibrosis in murine models, TREM2-deficient macrophages failed to acquire reparative phenotypes, showed impaired efferocytosis, and exacerbated fibrogenesis (36, 122–126).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [126]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“The finding of lipid droplet containing microglia in GRN−/− mice is corroborated by a recent study which showed that cultured progranulin-deficient macrophages exhibited increased foam cell formation, i.e. lipid droplet accumulation, compared to wild type macrophages49.”
From Lipid-droplet-accumulating microglia represent a dysfunctional and proinflammatory state in the aging brain (2020) · cites this paper as [49]
Experimental — accuracy not yet measuredIn the citing paper
“These monocyte-derived/bone marrow-dependent macrophages in NASH livers share striking similarities with macrophages in related extrahepatic compartments such as the bone marrow or adipose tissue,72,73 including a subset of “lipid-associated macrophages” with a unique metabolically activated phenotype.74”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [73]
In the citing paper
“Second, monocyte-derived macrophages replace liver resident Kupffer cells that normally clear iron, resulting in iron overload, oxidative stress, and activation of HSCs into myofibroblasts (70, 74-77).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [76]
In the citing paper
“In fatty liver, a novel subset of lipid-associated macrophages (LAMs) display a unique ability to metabolize lipids, but their contribution to fibrosis is unknown (70, 76).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [76]
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Marschallinger, J., Iram, T., Zardeneta, M., Lee, S. E., Lehallier, B., Haney, M. S., Pluvinage, J. V., Mathur, V., Hahn, O., Morgens, D. W., et al. (2020) · Nature Neuroscience · doi:10.1038/s41593-019-0566-1 · Cited by 1,384
“1 Gil-Perotin, S., Alvarez-Buylla, A. & Garcia-Verdugo, J. M. Identification and characterization of neural progenitor cells in the adult mammalian brain. Adv Anat Embryol Cell Biol 203, 1-101, ix (2009). 2 Bligh, E.”
Background
Metadata
- Authors
- Jaitin, D. A., Adlung, L., Thaiss, C. A., Weiner, A., Li, B., Descamps, H., Lundgren, P., Bleriot, C., Liu, Z., Deczkowska, A., Keren-Shaul, H., David, E., Zmora, N., Eldar, S. M., Lubezky, N., Shibolet, O., Hill, D. A., Lazar, M. A., Colonna, M., Ginhoux, F., Shapiro, H., Elinav, E., & Amit, I.
- Affiliations
- Weizmann Institute of Science (IL)
- University of Pennsylvania (US)
- Shanghai Jiao Tong University (CN)
- Tel Aviv University (IL)
- Tel Aviv Sourasky Medical Center (IL)
- Children's Hospital of Philadelphia (US)
- Washington University in St. Louis (US)
- Agency for Science, Technology and Research (SG)
- Corresponding author
- Elinav, Eran
- Amit, Ido
- ORCID
- Jaitin, Diego Adhemar
- Adlung, Lorenz
- Thaiss, Christoph A.
- Weiner, Assaf
- Li, Baoguo
- Descamps, Hélène
- Lundgren, Patrick
- Liu, Zhaoyuan
- Deczkowska, Aleksandra
- David, Eyal
- Zmora, Niv
- Eldar, Shai Meron
- Lubezky, Nir
- Shibolet, Oren
- Hill, David A.
- Lazar, Mitchell A.
- Colonna, Marco
- Ginhoux, Florent
- Shapiro, Hagit
- Elinav, Eran
- Amit, Ido
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2019-07
- Volume
- 178
- Issue
- 3
- Pages
- 686-698.e14
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC7068689
- OpenAlex
- W2955261360
- Cited by
- 1,377
- References
- 61
- Citations by year
- 2026: 243 · 2025: 244 · 2024: 229 · 2023: 218 · 2022: 170 · 2021: 152 · 2020: 97 · 2019: 20
- FWCI
- 83.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Chan Zuckerberg Initiative
- HHMI
- European Research Council (724471-HemTree2.0)
- Thompson Family Foundation
- MRA (509044)
- Foundation (703/15)
- Ernest and Bonnie Beutler Research Program for Excellence in Genomic Medicine
- Helen and Martin Kimmel
- NeuroMac DFG/Transregional Collaborative Research Center
- International Progressive MS Alliance
- NMSS (PA-1604-08459)
- Adelis Foundation
- Wolfson Foundation
- NIH (DK116668, DK49780)
- CHOP
- The Center for Applied Genomics
- Children's Hospital of Philadelphia
- Human Metabolic Tissue Bank
- Penn Diabetes Research Center (P30 NIH DK19525, P30-DK-019525)
- Edward Mallinckrodt, Jr. Foundation
- Agilent
- Global Probiotics Council
- PennCHOP Microbiome Program
- Penn Institute for Immunology
- Penn Center for Molecular Studies in Digestive and Liver Diseases (P30-DK-050306)
- Penn Skin Biology and Diseases Resource-based Center (P30-AR-069589)
- Gilead Sciences International Research Scholars Program in Liver Disease
- The V.R. Schwartz Research Fellow Chair
- Y. and R. Ungar
- Leona M. and Harry B. Helmsley Charitable Trust
- J.L. and V. Schwartz
- D.L. Schwarz
- Israel Science Foundation
- Helmholtz Foundation
- Bill and Melinda Gates Foundation
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- TREM2, lipid-associated macrophages, white adipose tissue, obesity, adipose tissue macrophages, metabolic homeostasis, adipocyte hypertrophy, hypercholesterolemia, impaired glucose tolerance, single-cell transcriptomics, macrophage origin, metabolic disorders
- MeSH terms
- Animals, Humans, Lipids, Macrophages, Membrane Glycoproteins, Mice, Inbred C57BL, Monocytes, Obesity, Receptors, Immunologic, Signal Transduction, Glucose Intolerance, Mice, Knockout, Intra-Abdominal Fat, Lipid Metabolism, Mice, Adipose Tissue, White, Single-Cell Analysis, Diet, High-Fat
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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