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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Natural Foxp3+ regulatory T cells inhibit Th2 polarization but are biased toward suppression of Th17-driven lung inflammation
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Natural Foxp3+ regulatory T cells inhibit Th2 polarization but are biased toward suppression of Th17-driven lung inflammation

机译：天然Foxp3 +调节性T细胞抑制Th2极化，但倾向于抑制Th17驱动的肺部炎症

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nTregs prevent autoimmunity and modulate immune and inflammatory responses to foreign antigens. CD4+Foxp3+ nTregs from DO11.10 mice were expanded ex vivo, and their effectiveness in suppressing the development of lung inflammatory responses, elicited by differentiated CD4+ T cells following antigen inhalation, was examined. Effector DO11.10 CD4+ Th2 cells, when adoptively transferred into BALB/c mice that subsequently inhaled OVA, elicited a pronounced pulmonary, eosinophilic inflammation. Surprisingly, the cotransfer of expanded nTregs failed to suppress the Th2-mediated airway inflammation. Nevertheless, expanded OVA-specific CD4+Foxp3+ nTregs were highly effective at inhibiting the polarization of na?ˉve CD4+ T cells into a Th2 phenotype. This suppression was reversed by an antibody to GITR but was not affected by the presence of the soluble OX40L. Further analysis revealed that although nTregs also failed to inhibit the lung neutrophilic inflammation induced by effector CD4+ Th1 cells, they markedly suppressed pulmonary inflammation elicited by CD4+ Th17 cells but not AHR. The suppression of the Th17-mediated response was evident from a striking reduction in the proportion of OVA-specific T cells expressing IL-17 and the numbers of neutrophils present in the airways of Th17 recipient mice. Collectively, these results demonstrate that expanded nTregs clearly limit the Th2 polarization process and that Th17-mediated inflammatory responses are particularly prone to the immunoregulatory properties of nTregs. These findings thus indicate that expanded nTregs are restrictive in their ability to suppress airway inflammatory processes and AHR.
机译：nTreg可防止自身免疫并调节对外源抗原的免疫和炎症反应。将来自DO11.10小鼠的CD4 + Foxp3 + nTregs进行离体扩增，并检查了它们在抑制吸入抗原后分化的CD4 + T细胞引起的肺部炎症反应中的有效性。当将效应物DO11.10 CD4 + Th2细胞过继转移到BALB / c小鼠中并随后吸入OVA时，会引起明显的肺部嗜酸性粒细胞炎症。令人惊讶的是，扩展的nTregs的共转移未能抑制Th2介导的气道炎症。然而，扩大的OVA特异性CD4 + Foxp3 + nTregs在抑制幼稚CD4 + T细胞极化为Th2表型方面非常有效。抑制作用被GITR抗体逆转，但不受可溶性OX40L的存在的影响。进一步的分析显示，尽管nTregs也不能抑制效应CD4 + Th1细胞诱导的肺嗜中性炎症，但它们显着抑制了CD4 + Th17细胞而非AHR引起的肺炎症。从表达IL-17的OVA特异性T细胞的比例和Th17受体小鼠气道中存在的中性粒细胞数量显着减少中可以明显看出Th17介导的反应受到抑制。这些结果共同表明，扩展的nTregs明显限制了Th2极化过程，并且Th17介导的炎症反应特别容易受到nTregs免疫调节特性的影响。因此，这些发现表明，扩展的nTregs在抑制气道炎性过程和AHR中的能力受到限制。

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