From
Ouroboros, a look at research into internal changes in
T cells with aging, some the mechanisms driving the
ongoing depletion of the naive T cell population, some not: "The
adaptive immune response requires waves of
T-cell clonal expansion on contact with altered self and contraction after elimination of
antigen. In the case of persisting antigen, as occurs for example
in cytomegalovirus or Epstein-Barr virus infection, this critical process can become dysregulated and responding T-cells enter into a dysfunctional
senescent state.
Longitudinal studies suggest that the presence of increased numbers of such T-cells is a poor prognostic factor for survival in the very elderly. ... These pathways and affected genes may play a significant role in driving the cellular senescent phenotype and warrant further investigation as potential biomarkers of aging and senescence. These genes may additionally provide targets for intervention. ... A possible mechanism for some age-related transcriptional changes is provided by Das et al., who describe the
negative effect of oxidation (both experimental and age-related) on the
proteasome. ... These results suggest that the decrease in proteasomal activities observed during aging may be secondary to
oxidative stress and underlie immune senescence."
View the Article Under Discussion:
http://ouroboros.wordpress.com/2007/02/16/2-on-t-age-related-changes-in-immune-cell-gene-expression-and-a-role-for-protein-oxidation/
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