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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Relative contributions of distinct MHC class cell populations in protection to tuberculosis infection in mice
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Relative contributions of distinct MHC class cell populations in protection to tuberculosis infection in mice

机译：独特的MHC类细胞群体对小鼠结核感染的保护作用的相对贡献

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A necessary role for cytotoxic T lymphocytes in protection against Mycobacterium tuberculosis (MTB) has been suggested by studies of the β2-microglobulin-deficient mouse, which is unable to present antigens through MHC class l and class l-like molecules and invariably succumbs early after infection. To identify the relative contributions of distinct putative MHC class l-dependent cell pop- ulations in protection against tuberculosis, we compared a variety of gene-disrupted mouse strains for susceptibility to MTB infection. Among the strains tested, the most susceptible mice, as measured by survival time and bacterial loads, were the β2-microglobulin-/-, followed by transporter associated with antigen processing defi- cient (TAP1-/-). CD8cr-/-. perforin-/-. and CD1d-/- mice. These findings indicated that (i) CD8+ T cells contribute to protection against MTB. and their protective activity is only partially depen- dent on perforin: (ii) β2-microglobulin-dependent T cell popula- tions distinct from CD~8+ T cells also contribute to anti-MTB immu- nity: and (iii) protective immune mechanisms are predominantly TAP-dependent. although TAP-independent mechanisms also con- tribute to protection. Because CD1d-deficient animals were fully resistant to MTB. other TAP-independent mechanisms must con- tribute to protection. We suggest here that both classical and nonclassical MHC class l-restricted T cells, distinct from CD1d- restricted cells, may be involved in protective immune responses against tuberculosis.
机译：β2-微球蛋白缺陷型小鼠的研究表明，细胞毒性T淋巴细胞在抵抗结核分枝杆菌（MTB）的保护中起着必要的作用，该小鼠无法通过MHC I类和I类分子提供抗原，并且总是在早期提早死亡。感染。为了确定不同的假定的MHC I类依赖细胞群在预防结核病中的相对作用，我们比较了多种基因破坏的小鼠品系对MTB感染的敏感性。在测试的菌株中，以存活时间和细菌载量衡量的最易感小鼠是β2-微球蛋白-/-，其次是与抗原加工缺陷相关的转运蛋白（TAP1-/-）。 CD8cr-/-。穿孔素-/-。和CD1d-/-小鼠。这些发现表明（i）CD8 + T细胞有助于针对MTB的保护。并且其保护活性仅部分取决于穿孔素：（ii）与CD〜8 + T细胞不同的β2-微球蛋白依赖性T细胞群也有助于抗MTB免疫：和（iii）保护性免疫机制主要取决于TAP。尽管独立于TAP的机制也有助于保护。因为缺乏CD1d的动物对MTB完全耐药。其他与TAP无关的机制也必须为保护做出贡献。我们在这里建议，与CD1d限制性细胞不同，经典和非经典的MHC I类限制性T细胞可能都参与了针对肺结核的保护性免疫应答。

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