Cellular, biochemical, and molecular basis of T-cell senescence.
The elucidation of age-related changes in immune functions is of great importance in light of the rising susceptibility of elderly individuals to infections, the likelihood that immunosenescence might also contribute to the age-related rise in cancer, and the role autoantibodies and immune complexes might play in general physical deterioration of aging individuals through their participation in subclinical chronic tissue damage. An attempt has been made to summarize our present knowledge on immune functions that are vulnerable to aging. It revealed that at the cellular level, all four antigen-responsive immune cells (T cells, B cells, monocytes, and killer cells) are vulnerable to aging, but T cells are perhaps the most vulnerable. Therefore, this article specifically examines the cellular and biochemical T cell-dependent concomitants of age-altered immune functions. One picture that is emerging suggests that at the molecular level, several control points exist along the path of gene expression that could be vulnerable to aging.
D000375:Aging / Q000276:immunology* / Q000378:metabolism; D002452:Cell Count; D002462:Cell Membrane / Q000502:physiology; D002467:Cell Nucleus / Q000648:ultrastructure; D003593:Cytoplasm / Q000378:metabolism; D006801:Humans; D007111:Immunity, Cellular; D007473:Ion Channels / Q000378:metabolism; D009243:NAD / Q000378:metabolism; D013601:T-Lymphocytes / Q000145:classification / Q000166:cytology / Q000502:physiology* / Q000648:ultrastructure; D014157:Transcription Factors / Q000378:metabolism
D007473:Ion Channels; D014157:Transcription Factors; D009243:NAD