Sadighi Akha Amir A, Miller Richard A
Department of Veterans Affairs Medical Center, Ann Arbor, Michigan 48109-0940, USA.
Curr Opin Immunol. 2005 Oct;17(5):486-91. doi: 10.1016/j.coi.2005.07.004.
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.
老年小鼠的T细胞在激活过程的早期阶段表现出缺陷，包括细胞骨架重组的改变，这种改变发生在T细胞受体区分激动剂和拮抗剂肽之前。衰老还会改变T细胞表面大分子的糖基化模式，对这些修饰的糖蛋白进行酶切可以恢复老年小鼠T细胞的高水平反应。质膜脂质和富含胆固醇的微结构域的改变也可能导致T细胞信号传导中与年龄相关的缺陷。老年B细胞内在信号缺陷的证据更为有限，但可能涉及激活转录因子E47的途径，该转录因子与体细胞超突变和类别转换重组有关。
