Hormones, genetic program and immunosenescence.
Immunosenescence is discussed in the context of an integrated immune-neuroendocrine homeostatic network. Under this new perspective, immunologic decline during aging appears as part of a multilevel phenomenon which affects intracellular as well as systemic regulatory mechanisms. In particular, the experimental data suggesting that during puberty, sex and adrenal steroids trigger thymus involution by inducing extensive apoptotic death of thymocytes is briefly reviewed. Next, the evidence indicating that aging brings about a progressive disruption in immune-neuroendocrine integration and the possible role of this disruption in the occurrence of age-associated autoimmune phenomena is considered. Finally, the possible mechanisms by which the genome can determine life span as well as the potential involvement of the major histocompatibility complex in this process are discussed.
Goya
R G
RG
Neuroendocrine Gerontology Unit, IMBICE, La Plata, Argentina.
D000375:Aging / Q000235:genetics / Q000276:immunology*; D000818:Animals; D017209:Apoptosis; D004393:Dwarfism, Pituitary / Q000188:drug therapy / Q000235:genetics / Q000276:immunology; D006728:Hormones / Q000627:therapeutic use; D006801:Humans; D007108:Immune Tolerance; D051379:Mice; D008817:Mice, Mutant Strains / Q000235:genetics / Q000276:immunology; D015213:Neuroimmunomodulation / Q000235:genetics; D009490:Neurosecretory Systems / Q000502:physiology; D011627:Puberty; D013950:Thymus Gland / Q000254:growth & development
D006728:Hormones