Aging of the immune system (immunosenescence) is characterized by diminished thymus function, decreased output of recent thymic emigrants, compensatory peripheral proliferation of mature T cells and oligoclonal expansions of specific CD28(-) T cells. Clinical consequences are poor responses to new antigens or vaccinations, increased infection rates with higher morbidity and mortality, and increasing incidence of autoimmune diseases with advancing age. Premature immunosenescence is suggested to play a role in the pathogenesis of adult rheumatoid arthritis and in children with juvenile idiopathic arthritis (JIA). However, so far, there is not enough evidence for supporting one of the two theories: the first, favoring premature immunosenscence in children developing autoimmune conditions as the primary defect causing break-down of self-tolerance; the second, that premature immunosenescence in children with autoimmune disorders is secondary to chronic stimulation and activation of the immune system by inflammatory processes by the autoimmune disease itself. This contradictory view of etiology and pathogenesis of autoimmune diseases in the very young underlines the need for population-based longitudinal studies on immune-risk factors for autoimmune diseases beginning at infancy.
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