Tuft cells, taste-chemosensory cells, orchestrate parasite type 2 immunity in the gut
Intestinal Diseases, Parasitic
TRPM Cation Channels
The intestinal epithelium forms an essential barrier separating host and microbiota. Protozoa and helminths are members of the gut microbiota of mammals, including humans; yet the many ways gut epithelial cells orchestrate responses to these Eukaryota remains unclear. Herein we show that tuft cells, taste-chemosensory epithelial cells, accumulate during parasite colonization and infection. Disruption of chemosensory signaling, via loss of Trpm5, abrogates expansion of tuft cells, goblet cells, eosinophils, and type-2 innate lymphoid cells (ILC2s) during parasite colonization. Tuft cells are the primary source of the parasite-induced cytokine, interleukin (IL)-25, which indirectly induces tuft cells expansion by promoting IL-13 production by ILCs. Our results identify intestinal tuft cells as critical sentinels in the gut epithelium, promote type-2 immunity in response to intestinal parasites.