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Oral γδT17 cells induced by macrophages-derived extracellular vesicles in peridontitis exacerbate rheumatoid arthritis

ABSTRACT: Periodontitis (PD) is one of the most common human inflammatory diseases, yet the immunological mechanism linking oral and systemic immune responses are not well defined. Here, we show that the accumulation of interleukin-17 (IL-17)-producing γδT (γδT17) cells occurs not only in the oral cavity, but also in the peripheral lymph nodes and spleens in experimental periodontitis in mice. Strikingly, oral γδT17 cells derived from experimental periodontitis migrated to the inflamed joint and led to an exacerbation of rheumatoid arthritis (RA) in a collagen-induced arthritis model in mice. Mechansitically, we demonstrated that the dysbiosis in periodontitis led to an increase in production of complement component 3 (C3)-enriched extracellular vesicles (EVs) derived from macrophages. These C3-enriched EVs were taken up by γδT cells and stimulated intracellular C3a receptor to drive IL-17A production in γδT cells. Our findings revealed an previously unrecognized immunological mechanism linking periodontitis to RA through the accumulation and migration of oral γδT17 cells.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Suspension Culture, Macrophage

DISEASE(S): Periodontitis

SUBMITTER: Wenzhe Wang

LAB HEAD: Bei Li

PROVIDER: PXD063380 | Pride | 2026-04-08

REPOSITORIES: Pride

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	0320TMTP3_1.raw	Raw
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