Abstract
T cells synthesize a large number of proteins during their development, activation, and differentiation. The build-up of misfolded and unfolded proteins in the endoplasmic reticulum, however, causes endoplasmic reticulum (ER) stress. Thus, T cells can maintain ER homeostasis via endoplasmic reticulum-associated degradation, unfolded protein response, and autophagy. In T cell-mediated diseases, such as rheumatoid arthritis, systemic lupus erythematosus, Sjogren's syndrome, type 1 diabetes and vitiligo, ER stress caused by changes in the internal microenvironment can cause disease progression by affecting T cell homeostasis. This review discusses ER stress in T cell formation, activation, differentiation, and T cell-mediated illnesses, and may offer new perspectives on the involvement of T cells in autoimmune disorders and cancer.
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