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首页> 外文期刊>Clinical and experimental allergy : >UV inhibits allergic airways disease in mice by reducing effector CD4 T cells.
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UV inhibits allergic airways disease in mice by reducing effector CD4 T cells.

机译：UV通过减少效应CD4 T细胞抑制小鼠过敏性气道疾病。

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BACKGROUND: In human asthma, and experimental allergic airways disease in mice, antigen-presenting cells and CD4(+) effector cells at the airway mucosa orchestrate, and CD4(+)CD25(+) regulatory T cells attenuate, allergen immunity. UV irradiation of skin before sensitization with ovalbumin (OVA) causes significantly reduced asthma-like responses in respiratory tissues. OBJECTIVE: To determine whether UV-induced changes in CD11c(+) cells, CD4(+)CD25(+) effector cells or CD4(+)CD25(+) regulatory cells in the trachea and airway draining lymph nodes (ADLNs) were responsible for reduced allergic airways disease. METHODS: The phenotype and function of CD11c(+) cells and CD4(+)CD25(+) cells in the trachea and ADLNs of UV- and non-irradiated, OVA-sensitized mice was examined 24 h after a single exposure to aerosolized OVA. RESULTS: No changes in the function of CD11c(+) cells from UV-irradiated mice were observed. CD4(+)CD25(+) cells from UV-irradiated, OVA-sensitized mice harvested 24 h after OVA aerosol proliferated less in response to OVA in vitro and were unable to suppress the proliferation of OVA-sensitized responder cells. This result suggested reduced activation of effector T cells in the airway mucosa of UV-irradiated, OVA-sensitized mice. To exclude regulatory cells of any type, there was similar proliferation in vivo to aerosolized OVA by CFSE-loaded, OVA-TCR-specific CD4(+) cells adoptively transferred into UV- and non-irradiated, OVA-sensitized mice. In addition, there was no difference in the expression of regulatory T cell markers (Foxp3, IL-10, TGF-beta mRNA). To examine effector T cells, ADLN cells from UV-irradiated, OVA-sensitized and -challenged mice were cultured with OVA. There was reduced expression of the early activation marker CD69 by CD4(+)CD25(+) cells, and reduced proliferation in the absence of the regulatory cytokine, IL-10. CONCLUSION: Reduced allergic airways disease in UV-irradiated mice is due to fewer effector CD4(+)CD25(+) cells in the trachea and ADLNs, and not due to UV-induced regulatory cells.
机译：背景：在人类哮喘和小鼠的实验性过敏性气道疾病中，气管粘膜组织的抗原呈递细胞和CD4（+）效应细胞以及CD4（+）CD25（+）调节性T细胞减弱了变应原免疫力。在卵清蛋白（OVA）致敏之前，紫外线照射皮肤会导致呼吸组织中的哮喘样反应明显减少。目的：确定是否紫外线引起CD11c（+）细胞，气管和气道引流淋巴结（ADLN）中的CD4（+）CD25（+）效应细胞或CD4（+）CD25（+）调节细胞的变化用于减少过敏性气道疾病。方法：对单次暴露于雾化的OVA后24 h的紫外线和未辐照的OVA致敏小鼠气管和ADLN中的CD11c（+）细胞和CD4（+）CD25（+）细胞表型和功能进行检查。结果：未观察到紫外线照射的小鼠CD11c（+）细胞功能的变化。在OVA气雾剂24小时后收获的紫外线照射的OVA致敏小鼠的CD4（+）CD25（+）细胞在体外对OVA的响应较少，并且不能抑制OVA致敏的应答细胞的增殖。该结果表明，紫外线照射的OVA致敏小鼠的气道粘膜中的效应T细胞活化减少。为了排除任何类型的调节细胞，通过CFSE加载的，OVA-TCR特异性CD4（+）细胞过继转移到UV和非辐照的OVA致敏小鼠体内，与雾化的OVA有相似的体内增殖。此外，调节性T细胞标志物（Foxp3，IL-10，TGF-βmRNA）的表达没有差异。为了检查效应T细胞，用OVA培养来自紫外线照射的，OVA致敏的和攻击的小鼠的ADLN细胞。 CD4（+）CD25（+）细胞减少了早期激活标记CD69的表达，并且在缺乏调节性细胞因子IL-10的情况下减少了增殖。结论：紫外线照射的小鼠过敏性气道疾病的减少是由于气管和ADLNs中的效应CD4（+）CD25（+）细胞减少，而不是由于紫外线诱导的调节细胞。

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