title: The endoplasmic reticulum stress response in immunity and autoimmunity.
abstract: Many exogenous sources of stress can lead to cell death. In recent years, endogenous cellular sources of stress have also been identified, including the stress that arises from the accumulation of unfolded proteins within a cell's endoplasmic reticulum (ER). To counterbalance this type of ER stress, higher eukaryotic cells possess a three-pronged signal-transduction pathway termed the unfolded-protein response (UPR). This Review focuses on the role of the UPR in the mammalian immune system and how manipulation of this complex signalling pathway may be of therapeutic benefit in human disease.
authors.affiliation: Department of Infectious Diseases and Immunology, Harvard School of Public Health, 651 Huntington Avenue, Boston, Massachusetts 02115, USA.
authors.forename: Derrich J
authors.initials: DJ
authors.lastname: Todd
authors.forename: Ann-Hwee
authors.initials: AH
authors.lastname: Lee
authors.forename: Laurie H
authors.initials: LH
authors.lastname: Glimcher
mesh_terms: D000818:Animals; D015551:Autoimmunity / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology; D004721:Endoplasmic Reticulum / Q000276:immunology*; D006801:Humans; D007109:Immunity / Q000276:immunology*; D017510:Protein Folding; D011506:Proteins / Q000276:immunology / Q000378:metabolism; D013312:Stress, Physiological
chemical_list: D011506:Proteins