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首页> 外文期刊>Infection and immunity >T-cell-mediated protection of mice against virulent Mycobacterium tuberculosis.
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T-cell-mediated protection of mice against virulent Mycobacterium tuberculosis.

机译：T细胞介导的小鼠抵抗强力结核分枝杆菌的保护。

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We sought to protect CBA mice against tuberculosis using in vivo transfer of a T-cell line previously shown to be capable of I-A-restricted recognition of peritoneal macrophages infected in vitro with Mycobacterium tuberculosis. This line induces total bacteriostasis in vitro. In mice that received 500 rads of irradiation 48 h before infection, the T-cell line caused significant prolongation of life when given intravenously with a challenge dose of 5 x 10(6) organisms. Similar experiments with two other T-cell lines showed that these lines offered no protection. Bacterial load at the time of death was inversely related to the time of survival. Thus, death occurred at a lower bacterial load in adoptively protected mice, implying the contribution of an immunopathological component in these animals. The protective T-cell line, which was CD4+ CD8-, had no effect on the rate of growth of strain BCG in CBA nuu mice or M. tuberculosis in fully T-cell-deprived mice. This could indicate that CD8+ cells play a role in this system or that there is a need for the recruitment of interleukin 2-producing cells in the recipient. Experiments with monoclonal antibodies to selectively deplete T-cell subsets in normal CBA mice showed that depletion of CD4+ cells strikingly shortened survival, whereas depletion of CD8+ cells did not. However, CD8-depleted mice died with a lower bacterial load than those found in nondepleted controls, and the lesions in CD8-depleted mice were histopathologically distinct. These results suggest that the CD8+ cells either down-regulate bacteriostasis or cause immunopathology in this model and that it is the CD4+ cells that are the major protective subset in long-term protection experiments.
机译：我们试图通过体内转移的T细胞系保护CBA小鼠免受结核病的侵袭，该T细胞系先前被证明能够I-A限制识别在体外感染结核分枝杆菌的腹膜巨噬细胞。该系在体外诱导总的抑菌作用。在感染前48小时接受500 rad辐射的小鼠中，当以5 x 10（6）个生物体的剂量静脉内给予T细胞系时，可显着延长寿命。用另外两个T细胞系进行的类似实验表明，这些系没有提供保护。死亡时的细菌负荷与生存时间成反比。因此，在过继保护的小鼠中，细菌以较低的细菌负荷发生死亡，这暗示着免疫病理成分对这些动物的贡献。保护性T细胞系CD4 + CD8-对CBA nu / nu小鼠中BCG菌株的生长速率或完全T细胞剥夺的小鼠结核分枝杆菌的生长速率没有影响。这可能表明CD8 +细胞在该系统中起作用，或者需要在受体中募集产生白介素2的细胞。用单克隆抗体选择性消耗正常CBA小鼠中T细胞亚群的实验表明，耗竭CD4 +细胞会显着缩短生存期，而耗竭CD8 +细胞则不会。但是，与未耗尽对照组相比，耗竭CD8的小鼠的细菌载量更低，并且在病理组织学上，耗竭CD8的小鼠的病变也很明显。这些结果表明，在该模型中，CD8 +细胞下调抑菌作用或引起免疫病理变化，而CD4 +细胞是长期保护实验中的主要保护子集。

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