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Glycolysis and Autoimmune Diseases: A Growing Relationship Publisher



Rezaei R1 ; Tahmasebi S2 ; Atashzar MR1, 3 ; Amani D1
Authors
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Authors Affiliations
  1. 1. Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  2. 2. Department of Immunology, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Department of Immunology, School of Medicine, Fasa University of Medical Sciences, Fasa, Iran

Source: Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology Published:2020


Abstract

Abstract—: Under homeostasis states, proliferation, differentiation and function of immune cells are efficiently regulated to not only support the protection against pathogens, but also to prevent the autoimmune attack against self-tissues. It is now authenticated that immune cell activation is engaged with intense alterations in cellular metabolism. Accumulating body of data indicated that alterations in the metabolism of immune cells have a tight association with the pathogenesis of autoimmune diseases. Aerobic glycolysis is a major element in activation and differentiation of T cells. It has been established that aerobic glycolysis plays an essential role in the various pathophysiological aspects of several autoimmune diseases. A new emerging field of the specialty “Immunometabolism” has been developed and holds promise to explore new therapeutic targets. With consideration of common profile of metabolic perturbation in autoimmune diseases, targeting of these metabolic dysregulation heralds a beginning of a new chapter in the treatment of autoimmune diseases. In this review, we set out to discuss how glycolysis pathway can affect autoreactive T-cell differentiation/functions and also describe the latest findings associated with glucose metabolism and autoimmune diseases. Finally, we introduce new therapeutic approaches that could potentially alter metabolic perturbation and correct the Th17/Treg imbalance in autoimmune diseases. © 2020, Pleiades Publishing, Ltd.