Thymic Senescence

Abstract

Thymic senescence develops in every person, although at different pace. Thymic senescence significantly lowers the production of naive T cells, leading to increased incidence of infections, cancer and autoimmune diseases. Certain external factors can accelerate thymic senescence. These include chemicals (copper-chelators), hor-mones (androgens), infections (viruses, fungi, protozoa). Others may slow the aging process of the thymus including perturbations to the hormonal (sex-steroid) system, genetic alterations (PPARgamma deficiency) or chemical compounds (PPARgamma antagonists). Thymic senescence research may provide insight to underlying molecular events and potentially appoint novel therapeutic targets for senescence interven-tion strategies. These hold promise to postpone thymus senescence and enhance T cell production. That would result in a decreased incidence of infections, cancer and autoimmune diseases, currently affecting the elderly. The attributed drop in healthcare costs and gain in quality of life share tremendous economic and social interest.