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Ullah et al., 2023)

10.1158/1541-7786.MCR-14-0165-T Mol

& Bates, D

Such high metabolic demand to produce and secrete insulin can render the -cells susceptible to exceeding ER protein folding capacity, in turn leading to accumulation of misfolded proteins and ER stress ( + T cells in both mouse models and human patients of T1D ( + and CD4 + T cells, respectively ( These -cell characteristics make them vulnerable to destruction, and this is exacerbated in the pathogenic conditions of T1D and T2D, in which there are increased levels of pro-inflammatory cytokines, reactive oxygen species (ROS) and nitric oxide (NO), which are especially detrimental since -cells have limited antioxidant defense capabilities ( in vitro studies, wherein cultured human islets exposed to high glucose were observed to secrete IL-1, with production increasing due to autocrine feedback ( Furthermore, -cells produce several chemokines: (i) C-C ligand 5 (CCL5), also named RANTES, (ii) C-X-C motif chemokine ligand 10 (CXCL10), also called IP-10, and (iii) C-C ligand 2 (CCL2), also termed monotype chemoattractant protein or MCP1 ( in vivo by environmental triggers (such as viral infections), causing inflammation and macrophage recruitment ( Collectively, these -cell vulnerabilities, along with the signals they release under conditions of stress within the islet microenvironment, can create a self-perpetuating cycle of -cell destruction, which is exacerbated in conjunction with pro-inflammatory immune cells ( Figure 2 )