| First Author | Papotto PH | Year | 2023 |
| Journal | Cell Rep | Pages | 112074 |
| PubMed ID | 36787741 | Mgi Jnum | J:334242 |
| Mgi Id | MGI:7446173 | Doi | 1016/j.celrep.2023.112074 |
| Citation | Papotto PH, et al. (2023) Maternal gammadelta T cells shape offspring pulmonary type 2 immunity in a microbiota-dependent manner. Cell Rep :112074 |
| abstractText | Immune development is profoundly influenced by vertically transferred cues. However, little is known about how maternal innate-like lymphocytes regulate offspring immunity. Here, we show that mice born from gammadelta T cell-deficient (TCRdelta(-/-)) dams display an increase in first-breath-induced inflammation, with a pulmonary milieu selectively enriched in type 2 cytokines and type 2-polarized immune cells, when compared with the progeny of gammadelta T cell-sufficient dams. Upon helminth infection, mice born from TCRdelta(-/-) dams sustain an increased type 2 inflammatory response. This is independent of the genotype of the pups. Instead, the offspring of TCRdelta(-/-) dams harbors a distinct intestinal microbiota, acquired during birth and fostering, and decreased levels of intestinal short-chain fatty acids (SCFAs), such as pentanoate and hexanoate. Importantly, exogenous SCFA supplementation inhibits type 2 innate lymphoid cell function and suppresses first-breath- and infection-induced inflammation. Taken together, our findings unravel a maternal gammadelta T cell-microbiota-SCFA axis regulating neonatal lung immunity. |
