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      Tuft cells, taste-chemosensory cells, orchestrate parasite type 2 immunity in the gut

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          Abstract

          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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          Author and article information

          Journal
          0404511
          7473
          Science
          Science
          Science (New York, N.Y.)
          0036-8075
          1095-9203
          6 June 2017
          04 February 2016
          18 March 2016
          26 July 2017
          : 351
          : 6279
          : 1329-1333
          Affiliations
          [1 ]Departments of Immunology and Infectious Diseases and Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA
          [2 ]Division of Gastroenterology, Tufts Medical Center, Boston, MA 02111, USA
          [3 ]Monell Chemical Senses Center, Philadelphia, PA 19104, USA
          [4 ]Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, New York, NY 10021, USA
          [5 ]Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142, USA
          [6 ]Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA
          Author notes
          []Corresponding author. wgarrett@ 123456hsph.harvard.edu
          [*]

          Present address: Department of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada.

          Article
          PMC5528851 PMC5528851 5528851 nihpa840783
          10.1126/science.aaf1648
          5528851
          26847546
          a1699aef-4d01-427d-8155-e40914b9fa92
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