Abstract:
:Pancreatic-islet inflammation contributes to the failure of β cell insulin secretion during obesity and type 2 diabetes. However, little is known about the nature and function of resident immune cells in this context or in homeostasis. Here we show that interleukin (IL)-33 was produced by islet mesenchymal cells and enhanced by a diabetes milieu (glucose, IL-1β, and palmitate). IL-33 promoted β cell function through islet-resident group 2 innate lymphoid cells (ILC2s) that elicited retinoic acid (RA)-producing capacities in macrophages and dendritic cells via the secretion of IL-13 and colony-stimulating factor 2. In turn, local RA signaled to the β cells to increase insulin secretion. This IL-33-ILC2 axis was activated after acute β cell stress but was defective during chronic obesity. Accordingly, IL-33 injections rescued islet function in obese mice. Our findings provide evidence that an immunometabolic crosstalk between islet-derived IL-33, ILC2s, and myeloid cells fosters insulin secretion.
journal_name
Immunityjournal_title
Immunityauthors
Dalmas E,Lehmann FM,Dror E,Wueest S,Thienel C,Borsigova M,Stawiski M,Traunecker E,Lucchini FC,Dapito DH,Kallert SM,Guigas B,Pattou F,Kerr-Conte J,Maechler P,Girard JP,Konrad D,Wolfrum C,Böni-Schnetzler M,Finke D,Ddoi
10.1016/j.immuni.2017.10.015subject
Has Abstractpub_date
2017-11-21 00:00:00pages
928-942.e7issue
5eissn
1074-7613issn
1097-4180pii
S1074-7613(17)30470-3journal_volume
47pub_type
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