Immunity aging. I. The chronic perduration of the thymus acute involution at puberty? Or the participation of the lymphoid organs and cells in fatal physiologic decline?
The author has focused the subject on the perduration of puberty thymus involution as a cause of immunity aging, a term in which he does not include senescence. The decrease between immune reactions against HIV1 at 25 years of age and those at 35 is considerable; the decrease is also indirectly revealed by spontaneous tumor exponentially growing incidence after 40 years in man and its equivalent, 16 months in mice: the immunity parameters indicate a regression correlated with this incidence growth. He regrets the neglect of suppressor cell and anti-idiotype problems by the basic immunologic research. Given the role of cofactors non specifically related to the antigen, such as that CD28 and its ligands, he suggests the interest to approach immunology via the science of chaos and fractals, which would be more appropriate than classical methodology to study highly complex phenomena on which apparently minimal interventions may induce considerable effects.
Mathé
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Institut de Cancérologie et d'Immunologie & Hôpital Suisse de Paris, France.
D000328:Adult; D000368:Aged; D000375:Aging / Q000276:immunology*; D000818:Animals; D016922:Cellular Senescence; D006801:Humans; D007109:Immunity / Q000502:physiology*; D008214:Lymphocytes / Q000276:immunology / Q000502:physiology*; D051379:Mice; D008875:Middle Aged; D011627:Puberty; D013950:Thymus Gland / Q000276:immunology / Q000502:physiology*