| First Author | Kishikawa S | Year | 2026 |
| Journal | Cell Rep | Volume | 45 |
| Issue | 9 | Pages | 117903 |
| PubMed ID | 42658676 | Mgi Jnum | J:391716 |
| Mgi Id | MGI:8406028 | Doi | 10.1016/j.celrep.2026.117903 |
| Citation | Kishikawa S, et al. (2026) Interleukin-17A-producing gammadelta T cells drive cognitive dysfunction in periodontitis. Cell Rep 45(9):117903 |
| abstractText | 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 Vgamma4(+) gammadelta 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-TCRgammadelta 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. |
