Commensal-specific T cell plasticity promotes rapid tissue adaptation to injury

TLDR

Commensal‑specific T cells in barrier tissues such as skin interact with resident microbes, driving responses that support host defense and tissue repair. Skin injury releases epithelial alarmins that license type‑17 T cells to produce type‑2 cytokines. These skin‑resident commensal‑specific IL‑17A‑producing CD4⁺ and CD8⁺ T cells coexpress transcription factors for both type‑17 and type‑2 programs, enabling them to mediate antimicrobial activity at homeostasis and rapidly switch to tissue repair upon injury. Harrison et al., Science, this issue p.

Abstract

Commensal-specific T cells are flexible Barrier tissues, like the skin, are sites where noninvasive commensal microbes constantly interact with resident T cells. These encounters can result in commensal-specific T cell responses that promote, for example, host defense and tissue repair. Harrison et al. show that subsets of skin-resident commensal-specific interleukin-17A–producing CD4 + and CD8 + T cells have a dual nature: They coexpress transcription factors that direct antagonistic antimicrobial (type 17) and antiparasite and pro–tissue repair (type 2) programs. When skin is damaged, epithelial cell alarmins license type 17 T cells to turn on type 2 cytokines. Thus, commensal-specific type 17 T cells can direct antimicrobial activity under homeostatic conditions but rapidly turn on tissue repair in the context of injury. Science , this issue p. eaat6280