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首页> 外文期刊>Infection and immunity >Phosphoantigen Presentation by Macrophages to Mycobacterium tuberculosis-Reactive Vγ9Vδ2+ T Cells: Modulation by Chloroquine
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Phosphoantigen Presentation by Macrophages to Mycobacterium tuberculosis-Reactive Vγ9Vδ2+ T Cells: Modulation by Chloroquine

机译：巨噬细胞向结核分枝杆菌反应性Vγ9Vδ2+ T细胞的磷酸抗原呈递：氯喹的调节。

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Vγ9Vδ2+ T cells (γδ T cells) are activated by Mycobacterium tuberculosis and recognize mycobacterial nonpeptide phosphoantigens. The role of antigen-presenting cells in the processing and presentation of phosphoantigens to Vγ9Vδ2+ T cells is not understood. We analyzed the role of macrophages for activation of γδ T cells by a new synthetic phosphoantigen bromohydrin pyrophosphate (BrHPP) and M. tuberculosis. Macrophages greatly increased γδ T-cell activation by both BrHPP and M. tuberculosis. Fixation of macrophages before infection demonstrated that uptake of M. tuberculosis was required for presentation to γδ T cells. Antigens of M. tuberculosis remained stably associated with macrophage surface and were not removed by paraformaldehyde fixation or washing. Macrophages processed M. tuberculosis for γδ T cells through a brefeldin A-insensitive pathway, suggesting that transport through the endoplasmic reticulum and Golgi complex of a putative presenting molecule is not important in the early processing of M. tuberculosis antigens for γδ T cells. Processing of M. tuberculosis was not eliminated by chloroquine, indicating that processing of γδ antigens is not dependent on acidic pH in the lysosomes. Chloroquine treatment of BrHPP-pulsed macrophages increased activation of γδ T cells. Ammonium chloride treatment of macrophages did not increase reactivity of γδ T cells to BrHPP, indicating that the effect of chloroquine was independent of pH changes in endosomes. Chloroquine, by inhibiting membrane traffic, may increase association and retention of phosphoantigens with cell surface membrane molecules on macrophages.
机译：Vem9Vδ2 + T细胞（γδT细胞）被结核分枝杆菌激活并识别分枝杆菌非肽磷酸抗原。目前尚不清楚抗原呈递细胞在磷酸抗原加工和呈递给Vγ9Vδ2 + T细胞中的作用。我们分析了巨噬细胞通过新型合成的磷酸抗原溴代醇焦磷酸盐（BrHPP）和 M激活γδT细胞的作用。结核病。巨噬细胞通过BrHPP和 M大大提高了γδT细胞的活化。结核病。感染前巨噬细胞的固定表明摄取 M。结核需要呈递给γδT细胞。 M抗原。结核病仍与巨噬细胞表面稳定结合，不能通过多聚甲醛固定或清洗而去除。巨噬细胞处理了 M。 γδT细胞通过布雷菲德菌素A不敏感的途径进入结核病，这表明假定的呈递分子通过内质网和高尔基复合体的转运在 M的早期加工中并不重要。 γδT细胞的结核抗原。 M的处理。氯喹未消除结核，表明γδ抗原的加工不依赖于溶酶体的酸性pH。 BrHPP脉冲巨噬细胞的氯喹处理增加了γδT细胞的活化。氯化铵处理巨噬细胞不会增加γδT细胞对BrHPP的反应性，表明氯喹的作用与内体的pH变化无关。通过抑制膜运输，氯喹可以增加磷酸抗原与巨噬细胞上细胞表面膜分子的缔合和保留。

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