期刊
SCIENCE
卷 351, 期 6279, 页码 1329-1333出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaf1648
关键词
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资金
- NUN National Research Service Award (NRSA) [F32DK098826]
- NIH NRSA [F31DK105653]
- NIH [R01 CA154426, R01 GM099531]
- Burroughs Wellcome Career in Medical Sciences Award
- Searle Scholars Award
The intestinal epithelium forms an essential barrier between a host and its microbiota. Protozoa and helminths are members of the gut microbiota of mammals, including humans, yet the many ways that gut epithelial cells orchestrate responses to these eukaryotes remain unclear. Here we show that tuft cells, which are taste-chemosensory epithelial cells, accumulate during parasite colonization and infection. Disruption of chemosensory signaling through the loss of TRMP5 abrogates the expansion of tuft cells, goblet cells, eosinophils, and type 2 innate lymphoid cells during parasite colonization. Tuft cells are the primary source of the parasite-induced cytokine interleukin-25, which indirectly induces tuft cell expansion by promoting interleukin-13 production by innate lymphoid cells. Our results identify intestinal tuft cells as critical sentinels in the gut epithelium that promote type 2 immunity in response to intestinal parasites.
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