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. 2022 Jan 13;12:798155. doi: 10.3389/fimmu.2021.798155

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Copyright © 2022 Palano, Cucchiara, Gallazzi, Riccio, Mortara, Gensini, Spinetti, Ambrosio and Bruno

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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NK cells in Type 2 diabetes. In humans, circulating NK cells in T2D subjects have been found to increase in number (A) but with decreased expression of both NKp46 and NKG2D activation markers, thus showing a reduced functionality (B). At the molecular level, circulating NK cells in T2D showed an increased mRNA expression of BiP, PDI, and sXBP1, a marker of unfolded protein response (UPR) which in turn is related to ER stress-activated by PERK and IRE1 sensors (C). These mechanisms are related to NKG2D down-modulation in circulating NK cells (C). In addition, NK cells showed an increased general DNA methylation (D). To mimic T2D mice are fed with high fat diet (HFD) (E) and within visceral adipose tissue, NK cells through IFNγ and TNFα release can induce macrophages polarization toward a pro-inflammatory M1-like phenotype thus promoting inflammation (E).