| First Author | Huang HI | Year | 2023 |
| Journal | Cell Rep | Volume | 42 |
| Issue | 8 | Pages | 112951 |
| PubMed ID | 37556321 | Mgi Jnum | J:339955 |
| Mgi Id | MGI:7525076 | Doi | 10.1016/j.celrep.2023.112951 |
| Citation | Huang HI, et al. (2023) A binary module for microbiota-mediated regulation of gammadelta17 cells, hallmarked by microbiota-driven expression of programmed cell death protein 1. Cell Rep 42(8):112951 |
| abstractText | Little is known about how microbiota regulate innate-like gammadelta T cells or how these restrict their effector functions within mucosal barriers, where microbiota provide chronic stimulation. Here, we show that microbiota-mediated regulation of gammadelta17 cells is binary, where microbiota instruct in situ interleukin-17 (IL-17) production and concomitant expression of the inhibitory receptor programmed cell death protein 1 (PD-1). Microbiota-driven expression of PD-1 and IL-17 and preferential adoption of a PD-1(high) phenotype are conserved for gammadelta17 cells across multiple mucosal barriers. Importantly, microbiota-driven PD-1 inhibits in situ IL-17 production by mucosa-resident gammadelta17 effectors, linking microbiota to their simultaneous activation and suppression. We further show the dynamic nature of this microbiota-driven module and define an inflammation-associated activation state for gammadelta17 cells marked by augmented PD-1, IL-17, and lipid uptake, thus linking the microbiota to dynamic subset-specific activation and metabolic remodeling to support gammadelta17 effector functions in a microbiota-dense tissue environment. |
