The Taste Receptor TAS1R3 Regulates Small Intestinal Tuft Cell Homeostasis
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23.full.pdf
Description
Published version
Size
2.33 MB
Format
Adobe PDF
Checksum (MD5)
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Author(s)
Howitt, Michael R
Cao, Y Grace
Gologorsky, Matthew B
Li, Jessica A
Haber, Adam L
Biton, Moshe
Lang, Jessica
Michaud, Monia
Regev, Aviv
Garrett, Wendy S
Date Issued
2020
Journal
ImmunoHorizons
Publisher
The American Association of Immunologists
Version
Final published version
Abstract
Tuft cells are an epithelial cell type critical for initiating type 2 immune responses to parasites and protozoa in the small intestine. To respond to these stimuli, intestinal tuft cells use taste chemosensory signaling pathways, but the role of taste receptors in type 2 immunity is poorly understood. In this study, we show that the taste receptor TAS1R3, which detects sweet and umami in the tongue, also regulates tuft cell responses in the distal small intestine. BALB/c mice, which have an inactive form of TAS1R3, as well as Tas1r3-deficient C57BL6/J mice both have severely impaired responses to tuft cell-inducing signals in the ileum, including the protozoa Tritrichomonas muris and succinate. In contrast, TAS1R3 is not required to mount an immune response to the helminth Heligmosomoides polygyrus, which infects the proximal small intestine. Examination of uninfected Tas1r3-/- mice revealed a modest reduction in the number of tuft cells in the proximal small intestine but a severe decrease in the distal small intestine at homeostasis. Together, these results suggest that TAS1R3 influences intestinal immunity by shaping the epithelial cell landscape at steady-state.
MIT Department
Howard Hughes Medical Institute
Koch Institute for Integrative Cancer Research at MIT
Massachusetts Institute of Technology. Department of Biology
Terms of Use
Creative Commons Attribution-NonCommercial-NoDerivs License
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DOI of Published Version
https://doi.org/10.4049/IMMUNOHORIZONS.1900099
