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JOURNAL ARTICLE

Gut-associated IgA + immune cells regulate obesity-related insulin resistance

Helen Luck, Saad Khan, Justin H Kim, Julia K Copeland, Xavier S Revelo, Sue Tsai, Mainak Chakraborty, Kathleen Cheng, Yi Tao Chan, Mark K Nøhr, Xavier Clemente-Casares, Marie-Christine Perry, Magar Ghazarian, Helena Lei, Yi-Hsuan Lin, Bryan Coburn, Allan Okrainec, Timothy Jackson, Susan Poutanen, Herbert Gaisano, Johane P Allard, David S Guttman, Margaret E Conner, Shawn Winer, Daniel A Winer
Nature Communications 2019 August 13, 10 (1): 3650
31409776
The intestinal immune system is emerging as an important contributor to obesity-related insulin resistance, but the role of intestinal B cells in this context is unclear. Here, we show that high fat diet (HFD) feeding alters intestinal IgA+ immune cells and that IgA is a critical immune regulator of glucose homeostasis. Obese mice have fewer IgA+ immune cells and less secretory IgA and IgA-promoting immune mediators. HFD-fed IgA-deficient mice have dysfunctional glucose metabolism, a phenotype that can be recapitulated by adoptive transfer of intestinal-associated pan-B cells. Mechanistically, IgA is a crucial link that controls intestinal and adipose tissue inflammation, intestinal permeability, microbial encroachment and the composition of the intestinal microbiome during HFD. Current glucose-lowering therapies, including metformin, affect intestinal-related IgA+ B cell populations in mice, while bariatric surgery regimen alters the level of fecal secretory IgA in humans. These findings identify intestinal IgA+ immune cells as mucosal mediators of whole-body glucose regulation in diet-induced metabolic disease.

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