title: Signal transduction in the aging immune system.
abstract: 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.
authors.affiliation: Department of Veterans Affairs Medical Center, Ann Arbor, Michigan 48109-0940, USA.
authors.forename: Amir A
authors.initials: AA
authors.lastname: Sadighi Akha
authors.forename: Richard A
authors.initials: RA
authors.lastname: Miller
mesh_terms: D000375:Aging; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D006801:Humans; D018448:Models, Immunological; D015398:Signal Transduction / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*