Shifts in immunometabolism in autoimmune diseases.

The immune system targets its own tissues in autoimmune disorders, chronic inflammatory syndromes that cause progressive damage and organ dysfunction. Psoriasis, multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus are amongst the conditions that are fuelled by excessive production of pro-inflammatory cytokines such as Tumor necrosis factor α (TNF-α), Interleukin 6 (IL-6), and Interleukin 17 (IL-17), as well as aberrant immune activation. Immunometabolism refers to the study of how metabolic pathways control immune cell activity and is associated with autoimmunity. The metabolic reprogramming that occurs during activation causes immune cells, including T cells, B cells, and macrophages, to switch from oxidative phosphorylation to glycolysis or glutaminolysis, which promotes increased cytokine release and rapid proliferation. In addition to maintaining the inflammatory response, this metabolic shift modulates the equilibrium between effector and regulatory cells, which increases autoimmunity. The chronic inflammation that characterizes autoimmune disorders is caused by the overproduction of cytokines in this altered metabolic state. This review offers fresh insights into the pathophysiology of autoimmunity by highlighting the importance of metabolic reprogramming in immune cells and its role in regulating cytokine production. Comprehensive insights into the metabolic pathway would reveal treatment opportunities that may help regulate abnormal cytokines and restore immunological balance.