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Article Abstract
Chemokine C-C motif ligand 7 (CCL7) is implicated in various immune and inflammatory processes; however, its role in rheumatoid arthritis (RA) remains unclear. In this study, we observed that CCL7 expression was upregulated in synovial M1-polarized macrophages and in the serum of RA mice and patients. CCL7 was found to promote macrophage polarization toward the M1 phenotype while inhibiting M2 differentiation . Furthermore, intra-articular injection of recombinant CCL7 protein in mice resulted in enhanced M1 polarization, increased inflammation, and fibrosis within synovial tissues, which exacerbated arthritis-associated pain. These effects were partially mitigated by treatment with a CCL7 neutralizing antibody. Mechanistically, we identified a CCL7 autocrine positive feedback loop that amplifies inflammation via the CCL7-CCR1-JAK2/STAT1 pathway. Collectively, our findings reveal a previously unrecognized CCL7-mediated autocrine inflammatory amplification loop that modulates macrophage polarization and exacerbates RA progression, positioning CCL7 as a potential therapeutic target for RA.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11987677 | PMC |
| http://dx.doi.org/10.1016/j.isci.2025.112177 | DOI Listing |
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