Guidi L, Antico L, Bartoloni C, Costanzo M, Errani A, Tricerri A, Vangeli M, Doria G, Gatta L, Goso C, Mancino L, Frasca D
Institute of Internal Medicine and Geriatrics, Catholic University, Rome, Italy.
Mech Ageing Dev. 1998 May 15;102(2-3):177-86. doi: 10.1016/s0047-6374(97)00144-9.
The effects of aging on the activation of the cytoplasmic tyrosine protein kinase p56(lck) have been investigated in PBL from adult and elderly subjects upon activation with mitogens or different co-stimuli. Results show that the amount and phosphorylation of p56(lck) are reduced in PBL from elderly as compared to adult subjects. This finding suggests that alterations in p56(lck) may contribute to the age-associated loss of some T cell functions, such as proliferation and IL-2 production, which are found decreased in PBL from old individuals. However, p56(lck) seems irrelevant to the production of IFN-gamma and IL-4 which were both found increased in the PBL from old subjects, as expected from the relative expansion of memory versus naive T cell subpopulations in aging.
在成年和老年受试者的外周血淋巴细胞（PBL）经丝裂原或不同共刺激激活后，研究了衰老对细胞质酪氨酸蛋白激酶p56(lck)激活的影响。结果显示，与成年受试者相比，老年受试者PBL中p56(lck)的量和磷酸化水平降低。这一发现表明，p56(lck)的改变可能导致与年龄相关的某些T细胞功能丧失，如增殖和白细胞介素-2产生，这些功能在老年个体的PBL中有所下降。然而，p56(lck)似乎与γ干扰素和白细胞介素-4的产生无关，正如预期的那样，衰老过程中记忆性T细胞亚群相对于初始T细胞亚群的相对扩增，老年受试者PBL中这两种细胞因子的产生均增加。
