Cellular immunity in aging.
Our study of the aging process in human beings and in mice is complicated by our need to know whether we are observing diseases of aging or natural nondisease state processes. Results from studies on inbred strains of mice and retrospective studies on HLA types in aging human populations suggest that genetic effects play a significant role in predetermining the life span of an individual. It is clear that in such mouse strains genetic defects that affect cell regulatory mechanisms result in the production of autoimmune reactivity, tumor development, and a shortened life span. In human beings, although results are less clear-cut, strong associations exist between some disease states and the HLA type. Also, the disappearance of HLA-B8 from older women suggests that this HLA type does not confer longevity. Cellular immune reactivity declines with age in all populations studied to date, and cell cooperative or regulatory mechanisms function less well. We need to characterize the specific nature of the cells directly responsible for these alterations and to attempt to correct deficiencies by dietary manipulation or transfer techniques.
D000375:Aging; D000818:Animals; D001323:Autoantibodies; D006801:Humans; D007111:Immunity, Cellular; D008285:Major Histocompatibility Complex; D051379:Mice; D008805:Mice, Inbred A; D008809:Mice, Inbred C3H; D008808:Mice, Inbred CBA; D008814:Mice, Inbred NZB; D013950:Thymus Gland / Q000166:cytology / Q000502:physiology
D001323:Autoantibodies