Inmunosenescencia y autoinmunidad: Mecanismos e implicaciones patológicas

Autoimmune diseases are chronic disorders characterized by the body's immune response against its own tissues, causing inflammation and tissue damage. Immunosenescence, a process associated with the aging of the immune system, has emerged as a crucial factor in the development and progression of these diseases. The mechanisms of premature immunosenescence shared by rheumatologic autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, inflammatory myopathies, systemic sclerosis, Sjögren's syndrome and vasculitis, are closely related to specific alterations in the T-lymphocyte population. There is a significant decrease in virgin T lymphocytes, which are essential for the primary adaptive immune response, while there is a marked increase in effector memory T lymphocytes, which are involved in secondary and persistent immune responses. In addition, there is an accumulation of immunosenescent cells that exhibit features of functional and proliferative impairment. These changes, together with mitochondrial dysfunction, epigenetic changes and telomere shortening, contribute significantly to the establishment and maintenance of a chronic inflammatory phenotype, characteristic of autoimmune diseases. Understanding these mechanisms is crucial for the development of new therapeutic strategies that address both autoimmunity and immunosenescence, especially given the need for more effective treatments in an aging population.