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首页> 外文期刊>The journal of immunology >CD11b+ Dendritic Cell–Mediated Anti–Mycobacterium tuberculosis Th1 Activation Is Counterregulated by CD103+ Dendritic Cells via IL-10
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CD11b+ Dendritic Cell–Mediated Anti–Mycobacterium tuberculosis Th1 Activation Is Counterregulated by CD103+ Dendritic Cells via IL-10

机译：CD11b +树突状细胞介导的抗结核分枝杆菌Th1激活被CD103 +树突状细胞通过IL-10调控。

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摘要

Mycobacterium tuberculosis , the pathogen causing pulmonary tuberculosis (TB) in humans, has evolved to delay Th1 immunity in the lung. Although conventional dendritic cells (cDCs) are known to be critical to the initiation of T cell immunity, the differential roles and molecular mechanisms of migratory CD11bsup+/sup and CD103sup+/sup cDC subsets in anti– M. tuberculosis Th1 activation remain unclear. Using a murine model of pulmonary M. tuberculosis infection, we found that slow arrival of M. tuberculosis –bearing migratory CD11bsup+/sup and CD103sup+/sup cDCs at the draining lymph nodes preceded the much-delayed Th1 immunity and protection in the lung. Contrary to their previously described general roles in Th polarization, CD11bsup+/sup cDCs, but not CD103sup+/sup cDCs, were critically required for Th1 activation in draining lymph nodes following M. tuberculosis infection. CD103sup+/sup cDCs counterregulated CD11bsup+/sup cDC–mediated Th1 activation directly by producing the immune-suppressive cytokine IL-10. Thus, our study provides new mechanistic insights into differential Th immune regulation by migratory cDC subsets and helps to develop novel vaccines and therapies.
机译：结核分枝杆菌是导致人类肺结核（TB）的病原体，已进化出可延迟肺中Th1免疫力的过程。尽管已知常规树突状细胞（cDCs）对于启动T细胞免疫至关重要，但迁移的CD11b + 和CD103 + cDC子集的不同作用和分子机制抗结核分枝杆菌Th1的激活仍不清楚。使用肺结核分枝杆菌感染的小鼠模型，我们发现携带结核分枝杆菌的迁徙性CD11b + 和CD103 + cDC缓慢到达引流淋巴结之前。大大延迟的Th1免疫力和对肺的保护作用。与先前描述的在Th极化中的一般作用相反，CD11b + cDCs，而不是CD103 + cDCs，对于结核分枝杆菌感染后引流淋巴结中的Th1激活至关重要。 。 CD103 + cDC通过产生免疫抑制性细胞因子IL-10直接调节CD11b + cDC介导的Th1激活。因此，我们的研究为迁移性cDC亚群提供了不同的Th免疫调节机制的新机制，并有助于开发新的疫苗和疗法。

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