Tet2 deficiency–induced expansion of monocyte-derived macrophages promotes liver fibrosis
Open accessAbstract
Clonal hematopoiesis driven by Tet2 deficiency in myeloid cells (TetΔMye) is prevalent in elderly individuals; however, the role of Tet2ΔMye in liver fibrosis pathogenesis remains elusive. In this study, we demonstrated that Tet2-deficient monocyte-derived macrophages (MDMs) promoted cellular expansion and elevated C–C motif chemokine ligand 2/8 (Ccl2/8) secretion by stabilizing their mRNAs through 5hmC-mediated alterations in RNA–protein interactions. These chemokines engaged with the upregulated C–C motif chemokine receptor (Ccr2/3) on Tet2−/− monocytes, forming a positive feedback loop that amplified pro-inflammatory MDMs (pMDMs) accumulation in liver. Tet2−/− pMDMs activated hepatic stellate cells through IL-6, driving extracellular matrix deposition and fibrotic progression. Pharmacological inhibition of Ccl2/Ccl8 with Bindarit attenuated MDMs accumulation and liver fibrosis, whereas combined therapy with Bindarit and IL-6 neutralization synergistically suppressed liver fibrosis in Tet2ΔMye mice and aged chimeric models recapitulating Tet2ΔMye-related myeloid hematopoiesis. These findings present the mechanism that Tet2ΔMye aggravates liver fibrosis and highlight MDMs depletion plus IL-6 neutralization as a promising therapy for liver fibrosis in patients with Tet2ΔMye-related myeloid hematopoiesis.
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In a Tet2-deficiency-driven liver fibrosis model, combined application of a CCL2/CCL8 inhibitor and an IL-6 neutralizing antibody synergistically inhibited monocyte recruitment and blocked their HSC-activating signal, more effectively attenuating fibrosis than either agent alone.
“For instance, in a Tet2-deficiency-driven liver fibrosis model, combined application of a CCL2/CCL8 inhibitor and an IL-6 neutralizing antibody synergistically inhibited monocyte recruitment and blocked their HSCs-activating signal, more effectively attenuating fibrosis than either agent alone (67).”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [67]
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Experimental — accuracy not yet measuredThese macrophages secrete IL-6 to activate HSCs, accelerating fibrosis.
“These macrophages secrete IL-6 to activate HSCs, accelerating fibrosis (67).”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [67]
Tet2 gene-deficient clonal hematopoiesis, common in the elderly, drives abnormal expansion of MoMFs via positive feedback loops like CCL2/CCR2.
“Tet2 gene-deficient clonal hematopoiesis, common in the elderly, drives the abnormal expansion of MoMFs via positive feedback loops like CCL2/CCR2.”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [67]
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- Authors
- Feng, J., Wu, B., Li, Y., Sun, P., Liu, Q., Xiao, Q., Cai, J.-B., Zheng, Y., Chen, H., Xu, Y., Liu, Y., Shi, G.-M., Tan, L., & Shi, Y. G.
- Affiliations
- Shanghai Medical College of Fudan University (CN)
- Tongji University (CN)
- Cornell University (US)
- Corresponding author
- Feng, Jiuxing
- Shi, Yujiang Geno
- ORCID
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2025-12-26
- Volume
- 223
- Issue
- 2
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC12755866
- OpenAlex
- W7117925228
- Semantic Scholar
- 1f84e7cd6f88482c0085c651f9e8c13886f68a70
- Cited by
- 6
- References
- 36
- Citations by year
- 2026: 6
- FWCI
- 3.37
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- The Journal of Experimental Medicine (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (publishedVersion, cc-by)
- Funders
- China Postdoctoral Science Foundation (KLF1340024, GZC20231944)
- Fudan University (JIH1340084Y, JIH1340107Y)
- National Natural Science Foundation of China (82073113)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- TET2 deficiency, liver fibrosis, monocyte-derived macrophages, clonal hematopoiesis, 5-hydroxymethylcytosine, RNA-protein interactions, hepatic stellate cells, interleukin-6, bindarit, aging, extracellular matrix deposition
- MeSH terms
- Animals, DNA-Binding Proteins, Humans, Liver, Liver Cirrhosis, Macrophages, Male, Mice, Inbred C57BL, Monocytes, Proto-Oncogene Proteins, Interleukin-6, Mice, Knockout, Cell Proliferation, Dioxygenases, Mice, Receptors, CCR2, Hepatic Stellate Cells
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