B and T lymphocyte attenuator regulates CD8+ T cell-intrinsic homeostasis and memory cell generation
B and T lymphocyte attenuator regulates CD8+ T cell-intrinsic homeostasis and memory cell generation
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DOI：
10.1038/ni1418
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发表时间：
2007-02-01
影响因子：
30.5
通讯作者：
Kaye, Jonathan
中科院分区：
文献类型：
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作者：
Krieg, Carsten;Boyman, Onur;Kaye, Jonathan
B和T淋巴细胞衰减因子（BTLA）是T细胞活化的负性调节因子，但其在体内的功能尚不清楚。在这里，我们发现缺乏全长BTLA或其配体（疱疹病毒进入介质）的小鼠，记忆性CD8（+）T细胞的数量增加。记忆性CD8（+）T细胞表型是由CD8（+）T细胞库的T细胞内在扰动引起的。在竞争性抗原特异性系统中，原始BTLA缺陷型CD8（+）T细胞比野生型细胞更有效地产生记忆。这种效应不依赖于应答抗原特异性T细胞群体的初始扩增。此外，BTLA负调节CD4（+）和CD8（+）T细胞的抗原非依赖性稳态扩增。这些结果强调了BTLA在体内限制T细胞活性的两个中心功能。
B and T lymphocyte attenuator (BTLA) is a negative regulator of T cell activation, but its function in vivo is not well characterized. Here we show that mice deficient in full-length BTLA or its ligand, herpesvirus entry mediator, had increased number of memory CD8(+) T cells. The memory CD8(+) T cell phenotype resulted from a T cell-intrinsic perturbation of the CD8(+) T cell pool. Naive BTLA-deficient CD8(+) T cells were more efficient than wild-type cells at generating memory in a competitive antigen-specific system. This effect was independent of the initial expansion of the responding antigen-specific T cell population. In addition, BTLA negatively regulated antigen-independent homeostatic expansion of CD4(+) and CD8(+) T cells. These results emphasize two central functions of BTLA in limiting T cell activity in vivo.