Abstract

Age is a major risk factor for autoimmunity, and many autoimmune conditions tend to occur more frequently in the second half of life, when thymic T cell production and vulnerability are at their lowest. For an autoimmune condition to develop, numerous forbearance checkpoints must fail, and several of those are susceptible to the vulnerable aging process. The selection of T cells with increased affinity for tone- or neoantigen and enhanced growth and survival parcels can result from homeostatic T cell proliferation, which is largely responsible for T cell loss during majority. Under lymphopenic conditions, these cells can develop a memory-like phenotype. Due to the expression of signaling and non-supervisory molecules, the accumulation of end-discerned effector T cells, either for idle contagions or specific fortone-antigen, has a low activation threshold or induces anseditious terrain with their capacity to be cytotoxic and to produce inordinate quantities of cytokines, thereby converting or amplifying autoimmune responses.