Several lines of evidence suggest that premature aging of the immune system may cause alterations in the peripheral T cell homeostasis making individuals vulnerable to triggers of autoimmunity. Childhood-onset autoimmunity may offer the investigation of these aspects in the setting of a young, relatively inexperienced immune system which is affected by an imbalance in thymic output, altered proportions of peripheral T cell subpopulations and proinflammatory cytokines. One hypothesis favors the idea that premature immunosenscence in childhood-onset autoimmunity is the primary defect causing breakdown of self-tolerance; another hypothesis postulates that premature immunosenescence in children with autoimmune disorders is secondary to chronic stimulation and activation of the immune system by inflammatory processes. Population-based longitudinal studies on risk factors for development of autoimmunity beginning at infancy are required to understand the pathogenetic factors, which lead to the breakdown of self-tolerance and perpetuation of inflammation, to allow the design of targeted therapy and preventive strategies.
Keywords: Immunosenescence, aging, autoimmunity, T cells, T cell receptor diversity, homeostasis, CMV, regulatory, interleukin-7, Autoimmune Diseases, immune system, cytokines, autoimmune disorders, inflammation, regulatory T cells, cytomegalovirus, rheumatoid arthritis, multiple sclerosis, CD28, T cell receptor, diabetes mellitus type I, thymocytes, recent thymic, Polymorphisms, autoimmune regulator, polyglandular syndrome, major histocompatibility, etiopathogenesis, TCR- chain, Telomeres, TTAGGG-rich, SLE, immunosuppression
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