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Pathogenic factors driving obesity to type 2 diabetes (T2D) are not fully understood. Group 1 innate lymphoid cells (ILC1s) are effectors of innate immunity and enriched in inflamed tissues. Here we show that the number of adipose ILC1s increases in obese T2D patients and correlates with glycemic parameters and with the number of ILC1s in the blood; circulating ILC1 numbers decrease as a result of metabolic improvements after bariatric surgery. In vitro co-culture experiments show that human adipose ILC1s promote adipose fibrogenesis and CD11c + macrophage activation. Reconstruction of the adipose ILC1 population in Prkdc −/− IL2rg −/− mice by adoptive transfer drives adipose fibrogenesis through activation of TGFβ1 signaling; however, transfer of Ifng −/− ILC1s has no effect on adipose fibrogenesis. Furthermore, inhibiting adipose accumulation of ILC1s using IL-12 neutralizing antibodies attenuates adipose tissue fibrosis and improves glycemic tolerance. Our data present insights into the mechanisms of local immune disturbances in obesity-related T2D.

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To enhance cell attachment and promote liver functions of hepatocytes cultured in bioreactors, a chitosan nanofiber scaffold was designed and prepared via electrospinning. Effects of the scaffold on hepatocyte adhesion, viability and function were then investigated. Data showed that hepatocytes on chitosan nanofiber scaffold exhibited better viability and tighter cell-substrate contact than cells on regular chitosan film. In addition, urea synthesis, albumin secretion and cytochrome P450 activity of hepatocytes on chitosan nanofiber scaffold were all 1.5 to 2 folds higher than the controls. Glycogen synthesis was also increased as compared with the controls. These results suggested the potential application of this chitosan nanofiber scaffold as a suitable substratum for hepatocyte culturing in bioreactors.