Interleukin-17A-producing γδ T cells drive cognitive dysfunction in periodontitis.

Authors

Sari Kishikawa, Jun-Ichi Nagao, Kenji Toyonaga, Aoba Iwanuma, Satoru Iwai, Arisa Aosaka, Yoshihiko Tanaka

Published in

Cell reports. Volume 45. Issue 9. Pages 117903. Aug 27, 2026. Epub Aug 27, 2026.

Abstract

Periodontitis, caused by the oral pathobiont Porphyromonas gingivalis (Pg), leads to progressive systemic diseases through oral-organ interactions, including cognitive dysfunction. However, the behavioral and immunological mechanisms underlying the oral-brain axis during the development of periodontitis remain unclear. We found that Pg-induced periodontitis promoted anxiety-like behavior and progressive cognitive dysfunction in mice. While Pg-induced periodontitis drove the accumulation of interleukin (IL)-17A-producing T cells in the mouth, an increased population of Vγ4⁺ γδ T cells migrate to the brain through the draining cervical lymph nodes via the CCL20/CCR6 pathway. Treatment with an anti-IL-17A antibody, an anti-CCL20 antibody, or anti-TCRγδ antibody ameliorated both anxiety-like behavior and cognitive dysfunction, and suppressed the increased expression of IL-17A receptor in the brain. Collectively, our findings reveal a function beyond its established role for IL-17A in the oral-brain axis that links Pg-induced periodontitis to cognitive dysfunction.

PMID:
42658676
Bibliographic data and abstract were imported from PubMed on 28 Aug 2026.

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