Harnessing the dual immunomodulatory function of myeloid-derived suppressor cells to reshape the inflammatory microenvironment for osteoarthritis therapy.

ABSTRACT: Osteoarthritis (OA) pathogenesis is profoundly influenced by dysregulated immune dynamics, where persistent interleukin-17 (IL-17)/T helper 17 (Th17) cell mediated inflammation coordinates with failed regenerative processes to perpetuate joint destruction. Here, we unveil the role of myeloid-derived suppressor cells (MDSCs) as dual-phase regulators that paradoxically orchestrate both inflammatory escalation and tissue repair in OA progression. Intra-articular administration of MDSCs in OA mice amplified IL-17 dependent inflammatory cascades and chemokine-driven leukocyte recruitment, revealing a context-dependent pro-inflammatory phenotype. Unexpectedly, MDSC depletion failed to attenuate joint damage, implying their indispensable yet multifaceted role in OA pathogenesis. Mechanistically,

SUBMITTER: Guo Z 

PROVIDER: S-EPMC12510078 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature