Does the immune system of a mouse age faster than the immune system of a human?
One of the characteristics of all somatic cells is a finite life span. Cells may proliferate until they reach a point after which, although they are metabolically active, they can no longer produce daughter cells. This observation is central to the clonal exhaustion hypothesis, a mechanism cited to explain age-associated immune dysfunction. In this hypothesis, repeated division of lymphocytes leads to a replicative limit, after which they enter the senescent phase but are not lost from the pool of T cells. Advancing age would then be associated with an increase in the number of T cells that are unable to proliferate to a stimulus which induces a proliferative response in T cells from younger individuals. This hypothesis seems both logical and reasonable and is supported by data from both humans and mice with the demonstration of an age-related accumulation of senescent T cells in both species. However, there is an apparent paradox. The paradox arises because the onset of immunosenescence appears to be more closely linked to the life span of the animal rather than the life span of the lymphocyte.
Department of Immunology, Imperial College School of Medicine at Chelsea and Westminster Hospital, London, UK. r.aspinall@ic.ac.uk
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D000375:Aging / Q000235:genetics / Q000276:immunology*; D000818:Animals; D016922:Cellular Senescence; D006801:Humans; D007107:Immune System / Q000276:immunology*; D051379:Mice; D008938:Mitosis; D013601:T-Lymphocytes / Q000276:immunology; D013950:Thymus Gland / Q000276:immunology; D013997:Time Factors