ASSESSMENT OF ALLOREACTIVE T-CELL SUBPOPULATIONS OF AGED MICE IN-VIVO - CD4+ BUT NOT CD8+ T-CELL-MEDIATED REJECTION RESPONSE DECLINES WITH ADVANCED AGE
ASSESSMENT OF ALLOREACTIVE T-CELL SUBPOPULATIONS OF AGED MICE IN-VIVO - CD4+ BUT NOT CD8+ T-CELL-MEDIATED REJECTION RESPONSE DECLINES WITH ADVANCED AGE
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DOI：
10.1002/eji.1830240611
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发表时间：
1994-06-01
影响因子：
5.4
通讯作者：
BLOOM, ET
中科院分区：
文献类型：
--
作者：
ROSENBERG, AS;SECHLER, JMG;BLOOM, ET
本研究探讨了在体内介导同种异体反应的T细胞群体中与年龄相关的改变。将主要组织相容性复合体（MHC）II类不同的bm 12皮肤（其排斥反应需要CD 4（+）T细胞）和MHC I类不同的bm 1皮肤（其排斥反应需要CD 8（+）T细胞）移植到健康的老年和年轻H-2（B）和H-2（B）xH-2（k）小鼠。与年轻小鼠相比，两种性别的老年小鼠bm 12皮肤移植物的存活时间延长，但对bm 1皮肤移植物的排斥率与年轻小鼠相当。与bm 12皮肤移植物的长期存活一致，在体外从老年小鼠的T细胞中引起Ia（bm 12）CTL活性的水平显著降低。然而，在来自老年小鼠T细胞的K-bm 1 CTL水平中没有观察到这种下降。Ia（bm 12）同种特异性应答的改变不能归因于老年小鼠的CD 4（+）T细胞的数量变化，并且向老年小鼠的应答培养物中添加可溶性T细胞辅助因子不能增加Ia（bm 12）细胞毒性T淋巴细胞活性。这些数据表明，衰老从根本上影响CD 4（+）T细胞介导的同种特异性应答，特别是在体内，并且仅可溶性T细胞辅助因子的产生缺陷不能解释这种缺陷。
The present investigation explored age-related alterations in T cell populations mediating allospecific responses in vivo. Healthy aged and young H-2(b) and H-2(b)xH-2(k) mice were engrafted with major histocompatibility complex (MHC) class II-disparate bm12 skin, rejection of which requires CD4(+) T cells, and MHC class I-disparate bm1 skin, rejection of which requires CD8(+) T cells. Aged mice of both genders exhibited prolonged survival of bm12 skin grafts relative to their young counterparts but rejected bm1 skin grafts at a rate equivalent to that of young mice. Consistent with prolonged survival of bm12 skin grafts, markedly diminished levels of Ia(bm12) CTL activity were elicited from T cells of aged mice in vitro. However, no such decline was observed in the level of K-bm1 CTL from T cells of aged mice. The alterations in Ia(bm12) allospecific responses were not attributable to quantitative changes in CD4(+) T cells of aged mice, and addition of soluble T cell helper factors to response cultures of aged mice did not augment Ia(bm12) cytotoxic T lymphocytes activity These data demonstrate that aging fundamentally affects CD4(+) T cell-mediated allospecific responses particularly in vivo, and that deficient generation of soluble T cell helper factors alone cannot explain this deficit.