Unknown

Dataset Information

0

MAIT cells are imprinted by the microbiota in early life and promote tissue repair.


ABSTRACT: How early-life colonization and subsequent exposure to the microbiota affect long-term tissue immunity remains poorly understood. Here, we show that the development of mucosal-associated invariant T (MAIT) cells relies on a specific temporal window, after which MAIT cell development is permanently impaired. This imprinting depends on early-life exposure to defined microbes that synthesize riboflavin-derived antigens. In adults, cutaneous MAIT cells are a dominant population of interleukin-17A (IL-17A)-producing lymphocytes, which display a distinct transcriptional signature and can subsequently respond to skin commensals in an IL-1-, IL-18-, and antigen-dependent manner. Consequently, local activation of cutaneous MAIT cells promotes wound healing. Together, our work uncovers a privileged interaction between defined members of the microbiota and MAIT cells, which sequentially controls both tissue-imprinting and subsequent responses to injury.

SUBMITTER: Constantinides MG 

PROVIDER: S-EPMC7603427 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

altmetric image

Publications


How early-life colonization and subsequent exposure to the microbiota affect long-term tissue immunity remains poorly understood. Here, we show that the development of mucosal-associated invariant T (MAIT) cells relies on a specific temporal window, after which MAIT cell development is permanently impaired. This imprinting depends on early-life exposure to defined microbes that synthesize riboflavin-derived antigens. In adults, cutaneous MAIT cells are a dominant population of interleukin-17A (I  ...[more]

Similar Datasets

| S-EPMC6899450 | biostudies-literature
| S-EPMC5367950 | biostudies-literature
2023-01-10 | GSE207348 | GEO
| S-EPMC5110023 | biostudies-literature
2017-09-20 | GSE93134 | GEO
| S-EPMC6908573 | biostudies-literature
2024-10-15 | GSE241697 | GEO
| S-EPMC8338998 | biostudies-literature
| S-EPMC3567342 | biostudies-literature
| S-EPMC9670188 | biostudies-literature