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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Different potentials of gamma delta T cell subsets in regulating airway responsiveness: V gamma 1+ cells, but not V gamma 4+ cells, promote airway hyperreactivity, Th2 cytokines, and airway inflammation.
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Different potentials of gamma delta T cell subsets in regulating airway responsiveness: V gamma 1+ cells, but not V gamma 4+ cells, promote airway hyperreactivity, Th2 cytokines, and airway inflammation.

机译：γ-δT细胞亚群在调节气道反应性方面具有不同的潜力：Vγ1+细胞而不是Vγ4+细胞促进气道高反应性，Th2细胞因子和气道炎症。

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摘要

Allergic airway inflammation and hyperreactivity are modulated by gammadelta T cells, but different experimental parameters can influence the effects observed. For example, in sensitized C57BL/6 and BALB/c mice, transient depletion of all TCR-delta(+) cells just before airway challenge resulted in airway hyperresponsiveness (AHR), but caused hyporesponsiveness when initiated before i.p. sensitization. Vgamma4(+) gammadelta T cells strongly suppressed AHR; their depletion relieved suppression when initiated before challenge, but not before sensitization, and they suppressed AHR when transferred before challenge into sensitized TCR-Vgamma4(-/-)/6(-/-) mice. In contrast, Vgamma1(+) gammadelta T cells enhanced AHR and airway inflammation. In normal mice (C57BL/6 and BALB/c), enhancement of AHR was abrogated only when these cells were depleted before sensitization, but not before challenge, and with regard to airway inflammation, this effect was limited to C57BL/6 mice. However, Vgamma1(+) gammadelta T cells enhanced AHR when transferred before challenge into sensitized B6.TCR-delta(-/-) mice. In this study Vgamma1(+) cells also increased levels of Th2 cytokines in the airways and, to a lesser extent, lung eosinophil numbers. Thus, Vgamma4(+) cells suppress AHR, and Vgamma1(+) cells enhance AHR and airway inflammation under defined experimental conditions. These findings show how gammadelta T cells can be both inhibitors and enhancers of AHR and airway inflammation, and they provide further support for the hypothesis that TCR expression and function cosegregate in gammadelta T cells.
机译：过敏气道炎症和反应过度受γδT细胞调节，但不同的实验参数会影响所观察到的效果。例如，在致敏的C57BL / 6和BALB / c小鼠中，气道攻击之前所有TCR-delta（+）细胞的短暂消耗都会导致气道高反应性（AHR），但在腹膜内注射之前引发低反应性。敏化。 Vgamma4（+）γT细胞强烈抑制AHR。它们的耗竭缓解了在激发之前而不是敏化之前开始的抑制作用，并且在激发之前转移到敏化的TCR-Vgamma4（-/-）/ 6（-/-）小鼠中时抑制了AHR。相反，Vgamma1（+）γT细胞增强了AHR和气道炎症。在正常小鼠（C57BL / 6和BALB / c）中，仅当这些细胞在致敏前被消耗掉而不是攻击之前就被消耗掉，AHR的增强才被消除，并且就气道炎症而言，这种作用仅限于C57BL / 6小鼠。但是，Vgamma1（+）gammadelta T细胞在攻击之前转移到致敏的B6.TCR-delta（-/-）小鼠中时增强了AHR。在这项研究中，Vgamma1（+）细胞还增加了气道中Th2细胞因子的水平，并在较小程度上增加了肺嗜酸性粒细胞的数量。因此，在定义的实验条件下，Vgamma4（+）细胞抑制AHR，而Vgamma1（+）细胞增强AHR和气道炎症。这些发现表明，γT细胞如何既可以作为AHR和气道炎症的抑制剂又可以作为增强剂，并且它们为TCR表达和功能在γT细胞中共同分离的假说提供了进一步的支持。

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