The endoplasmic reticulum stress response in immunity and autoimmunity

By D. Todd, Ann-Hwee Lee, Laurie H. Glimcher. Nature reviews. Immunology, 2008

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Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “This type of cellular stress originates from the accumulation of unfolded or misfolded proteins in the ER and usually triggers an adaptive response aimed at resolving ER stress, the UPR.(86) The UPR is mediated by at least three different stress-sensing pathways including pancreatic ER kinase (PERK)”
Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities (2008, background): “However, other mechanisms probably also contribute to the initiation of the UPR, including direct activation of some UPR signalling proteins by unfolded proteins (reviewed by Ref”
Nutrient sensing and inflammation in metabolic diseases (2008, background): “The UPR is mediated by three different stress-sensing pathways that are initiated by three transmembrane proteins which are located in the ER: pancreatic ER kinase ( PERK ; also known as EIF2AK3), inositol-requiring kinase 1 ( IRE1 ; also known as ERN1) and activating transcription factor 6 ( ATF6”
Impact of Obesity and Metabolic Syndrome on Immunity. (2016, background): “Immune cells must be ready to respond to any potential damaging pathogenic stimuli that may be encountered throughout the lifetime while also being able to carefully distinguish between “pathogen” and “self,” thereby preventing the incidence of autoimmune disorders (27, 32).”