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Blockade of IL-6 signaling alleviates atherosclerosis in Tet2-deficient clonal hematopoiesis
Open accessAbstract
Clonal hematopoiesis (CH) increases the risk of atherosclerotic cardiovascular disease possibly due to increased plaque inflammation. Human studies suggest that limitation of interleukin-6 (IL-6) signaling could be beneficial in people with large CH clones, particularly in TET2 CH. Here we show that IL-6 receptor antibody treatment reverses the atherosclerosis promoted by Tet2 CH, with reduction of monocytosis, lesional macrophage burden and macrophage colony-stimulating factor 1 receptor (CSF1R) expression. IL-6 induces expression of Csf1r in Tet2-deficient macrophages through enhanced STAT3 binding to its promoter. In mouse and human Tet2-deficient macrophages, IL-6 increases CSF1R expression and enhances macrophage survival. Treatment with the CSF1R inhibitor PLX3397 reversed accelerated atherosclerosis in Tet2 CH mice. Our study demonstrates the causality of IL-6 signaling in Tet2 CH accelerated atherosclerosis, identifies IL-6-induced CSF1R expression as a critical mechanism and supports blockade of IL-6 signaling as a potential therapy for CH-driven cardiovascular disease. Liu et al. report that the IL-6R antibody reduces the atherosclerosis promoted by Tet2 clonal hematopoiesis (CH) via reversal of increased macrophage colony-stimulating factor 1 receptor expression and suggests blocking IL-6 signaling as a potential therapy for CH-driven cardiovascular disease.
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TL;DR
In a mouse model of Tet2-deficient clonal hematopoiesis, IL-6 receptor blockade reversed accelerated atherosclerosis, monocytosis, lesional macrophage burden, and CSF1R expression. The proposed mechanism is IL-6-induced STAT3 binding to the Csf1r promoter in Tet2-deficient macrophages, increasing CSF1R-dependent macrophage survival; CSF1R inhibition also reversed atherosclerosis.
Key findings
- IL-6R antibody treatment in Tet2 CH mice reversed monocytosis, reduced aortic monocytes/macrophages, eliminated the significant increase in aortic root lesion area, reversed increased lesional macrophage staining, and increased fibrous cap area; it did not alter necrotic core area or lesional IL-1β.
- Tet2 CH increased CSF1R staining in lesional macrophages and on bone marrow monocytes, and increased CSF1R expression in HSPC subsets; IL-6R antibody reversed these increases.
- In Tet2-deficient macrophages, IL-6 increased Csf1r mRNA and STAT3 binding to the Csf1r promoter; increased nuclear acetylated STAT3 was observed, and HDAC inhibition with TSA increased STAT3 acetylation, promoter binding, and Csf1r mRNA in control macrophages.
- CSF1R inhibitor PLX3397 reduced circulating Ly6Chi, Ly6Clo, and total monocytes and completely reversed accelerated atherosclerosis in Tet2 CH mice; in humans with TET2 CH (n = 6) versus healthy individuals (n = 8), CD16+ monocytes showed 1.58-fold higher CSF1R expression (log2 fold change = 0.66, P = 0.0002), with CSF1R positivity in 59% versus 29%.
Methods
- Lethally irradiated Ldlr−/− mice were transplanted with 40% CD45.2 Tet2-deficient bone marrow plus 60% CD45.1 WT bone marrow (Tet2 CH) or control bone marrow, fed a Western diet, and treated with IL-6R-blocking antibody or IgG; a separate cohort received the CSF1R inhibitor PLX3397.
- Mechanistic studies used mouse bone marrow-derived macrophages, Tet2-deficient and control cells, IL-6 treatment, ChIP–qPCR for STAT3 binding to the Csf1r promoter, methylated DNA capture, immunoblotting, flow cytometry, and apoptosis/viability assays.
- Human relevance used CRISPR–Cas9-generated TET2−/− human ESCs and TET2+/− iPSCs differentiated into HSPCs and macrophages, plus scRNA-seq and targeted sequencing of PBMCs from patients with TET2 CH and controls.
Limitations
- The paper states that tocilizumab did not significantly alter CVD risk in the ENTRACTE trial and that tocilizumab raises LDL cholesterol and triglycerides, which may offset benefit; it also notes that Ldlr−/− mice avoid the IL-6-induced reduction in LDLR that may occur in humans.
- The paper states species differences in basal CSF1R protein levels and Akt phosphorylation between mouse and human macrophages, and that the human validation cohort was small (n = 6 TET2 CH, n = 8 healthy); it also states the study was not powered for sex-specific analyses.
- Evident from the text: the causal evidence is primarily from mouse models and cell systems, with no randomized clinical trial of IL-6 or CSF1R blockade in TET2 CH, and the human data are observational and limited in sample size.
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“Treatment with the CSF1R inhibitor PLX3397 reversed accelerated atherosclerosis in Tet2 CH mice.”
§ Blockade of IL-6 signaling alleviates atherosclerosis in Tet2-deficient clonal hematopoiesis > Abstract
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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
“Here we show that IL-6 receptor antibody treatment reverses the atherosclerosis promoted by Tet2 CH, with reduction of monocytosis, lesional macrophage burden and macrophage colony-stimulating factor 1 receptor (CSF1R) expression.”
§ Blockade of IL-6 signaling alleviates atherosclerosis in Tet2-deficient clonal hematopoiesis > Abstract
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“Here we show that IL-6 receptor antibody treatment reverses the atherosclerosis promoted by Tet2 CH, with reduction of monocytosis, lesional macrophage burden and macrophage colony-stimulating factor 1 receptor (CSF1R) expression.”
§ Blockade of IL-6 signaling alleviates atherosclerosis in Tet2-deficient clonal hematopoiesis > Abstract
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“Here we show that IL-6 receptor antibody treatment reverses the atherosclerosis promoted by Tet2 CH, with reduction of monocytosis, lesional macrophage burden and macrophage colony-stimulating factor 1 receptor (CSF1R) expression.”
§ Blockade of IL-6 signaling alleviates atherosclerosis in Tet2-deficient clonal hematopoiesis > Abstract
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“Here we show that IL-6 receptor antibody treatment reverses the atherosclerosis promoted by Tet2 CH, with reduction of monocytosis, lesional macrophage burden and macrophage colony-stimulating factor 1 receptor (CSF1R) expression.”
§ Blockade of IL-6 signaling alleviates atherosclerosis in Tet2-deficient clonal hematopoiesis > Abstract
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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In the paper
§ Blockade of IL-6 signaling alleviates atherosclerosis in Tet2-deficient clonal hematopoiesis > Results > TET2−/− macrophages show higher CSF1R and resist apoptosis
“in individuals with TET2 CH (n = 6), we found a 1.58-fold higher CSF1R expression among CD16+ monocytes (log2 fold change = 0.66, P = 0.0002), the major monocyte subset expressing CSF1R in humans69, compared to healthy individuals (n = 8)”
§ Blockade of IL-6 signaling alleviates atherosclerosis in Tet2-deficient clonal hematopoiesis > Methods > Human sample DNA extraction and CH variant calling
“CHIP mutations were determined via targeted capture panel, resulting in eight TET2 and six control patients.”
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Metadata
- Authors
- Liu, W., Yalcinkaya, M., Maestre, I. F., Olszewska, M., Ampomah, P. B., Heimlich, J. B., Wang, R., Vela, P. S., Xiao, T., Bick, A. G., Levine, R., Papapetrou, E. P., Libby, P., Tabas, I., Wang, N., & Tall, A. R.
- Affiliations
- Columbia University (US)
- Tisch Cancer Institute (US)
- Vanderbilt University Medical Center (US)
- Memorial Sloan Kettering Cancer Center (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Liu, Wenli
- Wang, Nan
- Tall, Alan R.
- ORCID
- Venue
- Nature Cardiovascular Research
- Published
- 2023-06-08
- Volume
- 2
- Issue
- 6
- Pages
- 572-586
- ISSN
- 2731-0590 (ISSN-L)
- PMC
- PMC10399458
- OpenAlex
- W4379878248
- Semantic Scholar
- 3bd13f920fde1647aafffc476ad7e87004a4a6bc
- Cited by
- 93
- References
- 86
- Citations by year
- 2026: 35 · 2025: 37 · 2024: 15 · 2023: 6
- FWCI
- 9.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Cardiovascular Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Fondation Leducq (TNE‐18CVD04, 18CVD04)
- Novo Nordisk
- National Institutes of Health
- Genentech
- National Heart, Lung, and Blood Institute (TNE-18CVD04, R01HL118567, R01HL134892, R01HL155431, R35HL145228, R01HL148071, R01HL163099)
- National Cancer Institute (P30CA008748)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Keywords
- clonal hematopoiesis, TET2 deficiency, atherosclerosis, IL-6 signaling, IL-6 receptor antibody, CSF1R, macrophages, STAT3, PLX3397, cardiovascular disease, plaque inflammation, monocytosis
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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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