The Skinny: Pancreatic ILC2s Promote Insulin Secretion

Kelly M Cautivo; Ari B Molofsky

doi:10.1016/j.immuni.2017.11.004

The Skinny: Pancreatic ILC2s Promote Insulin Secretion

Immunity. 2017 Nov 21;47(5):812-814. doi: 10.1016/j.immuni.2017.11.004.

Authors

Kelly M Cautivo¹, Ari B Molofsky²

Affiliations

¹ Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA; Diabetes Center, University of California, San Francisco, San Francisco, CA 94143, USA; Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA.
² Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA; Diabetes Center, University of California, San Francisco, San Francisco, CA 94143, USA; Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA. Electronic address: [email protected].

PMID: 29166583
DOI: 10.1016/j.immuni.2017.11.004

Abstract

Regulation of pancreatic insulin production is pivotal in the pathophysiology and treatment of diabetes. In this issue of Immunity, Dalmas et al. (2017) describe a type 2 immune circuit where pancreatic interleukin-33 (IL-33) promotes insulin secretion via the activity of islet-associated group 2 innate lymphoid cells (ILC2s).

Publication types

Comment

MeSH terms

Immunity, Innate*
Insulin Secretion
Interleukin-33*
Lymphocytes
Myeloid Cells
Tretinoin

Substances

Interleukin-33
Tretinoin