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首页> 外文期刊>Cellular immunology >Defects in apoptosis increase memory CD8+ T cells following infection of Bim-/-Faslpr/lpr mice.
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Defects in apoptosis increase memory CD8+ T cells following infection of Bim-/-Faslpr/lpr mice.

机译：Bim-/-Faslpr / lpr小鼠感染后，凋亡缺陷增加了记忆CD8 + T细胞。

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摘要

During many infections, large numbers of effector CD8(+) T cells are generated. After pathogen clearance, the majority of these cells undergo apoptosis, while the survivors differentiate into memory CD8(+) T cells. Although loss of both Bim and Fas function dramatically increased antigen-specific CD8(+) T cells in the lymph nodes following acute lymphocytic choriomeningitis virus (LCMV) infection, it was unclear whether they were pardoned effector or true memory CD8(+) T cells. In this study, we demonstrate they are bona fide memory T cells as characterized by surface marker expression, cytokine production, homeostatic proliferation, and ability to clear a secondary challenge of pathogen. Loss of both Bim and Fas also increased the number of virus-specific CD4(+) T cells found in the lymph nodes compared to the parental genotypes or wildtype mice. These studies illustrate that decreasing apoptosis increases the number of memory T cells and therefore could increase the efficacy of vaccines.
机译：在许多感染过程中，会产生大量的效应CD8（+）T细胞。病原体清除后，这些细胞中的大多数经历凋亡，而幸存者分化为记忆CD8（+）T细胞。虽然Bim和Fas功能的丧失都大大增加了急性淋巴细胞性脉络膜脑膜炎病毒（LCMV）感染后淋巴结中的抗原特异性CD8（+）T细胞的数量，但尚不清楚它们是原谅的效应子还是真正的记忆CD8（+）T细胞。在这项研究中，我们证明了它们是真正的记忆性T细胞，其特征在于表面标记物的表达，细胞因子的产生，体内稳态的增殖以及清除病原体继发攻击的能力。与亲本基因型或野生型小鼠相比，Bim和Fas的丢失也增加了在淋巴结中发现的病毒特异性CD4（+）T细胞的数量。这些研究表明减少的细胞凋亡增加了记忆T细胞的数量，因此可以提高疫苗的效力。

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