期刊
CURRENT OPINION IN IMMUNOLOGY
卷 17, 期 5, 页码 486-491出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2005.07.004
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- NIA NIH HHS [AG19619, AG08808] Funding Source: Medline
T cells from aged mice show defects in the early stages of the activation process, including alterations in cytoskeletal reorganization that precede discrimination, by the T cell receptor, of agonist from antagonist peptides. Aging also modifies the pattern of glycosylation of T cell surface macromolecules, and enzymatic cleavage of these modified glycoproteins can restore high level responses to T cells from aged mice. Alterations in plasma membrane lipids and cholesterol-rich microdomains might also contribute to age related deficits in T cell signaling. Evidence for intrinsic signal defects in aged B cells is more limited, but might involve pathways that activate the transcription factor E47, which has been implicated in somatic hypermutation and class-switch recombination.
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