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首页> 外文期刊>Clinical and experimental allergy : >Pulmonary allergic responses augment interleukin-13 secretion by circulating basophils yet suppress interferon-alpha from plasmacytoid dendritic cells.
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Pulmonary allergic responses augment interleukin-13 secretion by circulating basophils yet suppress interferon-alpha from plasmacytoid dendritic cells.

机译：肺过敏反应通过循环嗜碱细胞增加白介素13分泌，但抑制浆细胞样树突状细胞的干扰素-α。

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摘要

BACKGROUND: Allergic inflammatory processes may have the capacity to propagate systemically through the actions of circulating leucocytes. Consequently, basophils from allergic individuals are often 'primed', as evidenced by their hyperresponsiveness in vitro. IFN-alpha secreted predominantly by plasmacytoid dendritic cells (pDCs), suppresses basophil priming for IL-13 production in vitro. OBJECTIVE: This study sought in vivo correlates arising during experimental allergen challenge that support an 'axis-interplay' between basophils and pDCs. METHODS: Using segmental allergen challenge (SAC) in the lung, the immune responses of both cell types from the blood were investigated in volunteers (n=10) before and 24 h after allergen exposure. These responses were then correlated with inflammatory parameters measured in bronchoalveolar lavage fluids (BALF). RESULTS: In the blood, SAC significantly augmented IL-13 secretion by basophils induced by IL-3 (P=0.009), yet reduced IFN-alpha secreted by pDCs stimulated with CpG (P=0.018). Both parameters were negatively correlated (P=0.0015), at least among those subjects that secreted the latter. Circulating basophil IL-13 responses further correlated with post-SAC bronchoalveolar lavage (BAL) parameters including IL-13 protein (P=0.04), basophil (P=0.051), eosinophil (P=0.0018), and total cell counts (P<0.003). Basophil and IL-13 levels in BAL correlated likewise (P=0.0002). CONCLUSIONS: These results support a mechanism of immune regulation whereby an allergen reduces innate immune responses and IFN-alpha production by pDCs, resulting in an enhanced inflammation and basophil cytokine production at sites of allergen exposure.
机译：背景：过敏性炎症过程可能具有通过循环白细胞的作用全身传播的能力。因此，来自过敏性个体的嗜碱性粒细胞通常是“致敏的”，如其体外高反应性所证明的。主要由浆细胞样树突状细胞（pDC）分泌的IFN-α抑制了嗜碱性粒细胞在体外产生IL-13的启动作用。目的：本研究寻求在实验性变应原攻击过程中产生的体内相关性，以支持嗜碱性粒细胞和pDC之间的“轴相互作用”。方法：使用分段性过敏原激发（SAC）在肺中，在暴露于过敏原之前和之后24 h的志愿者（n = 10）中研究了两种细胞的血液免疫反应。然后将这些反应与在支气管肺泡灌洗液（BALF）中测得的炎症参数相关联。结果：在血液中，SAC显着增加了IL-3诱导的嗜碱性粒细胞的IL-13分泌（P = 0.009），但降低了CpG刺激的pDC分泌的IFN-α（P = 0.018）。至少在分泌后者的那些受试者中，这两个参数均呈负相关（P = 0.0015）。循环中的嗜碱性粒细胞IL-13反应进一步与SAC后支气管肺泡灌洗（BAL）参数相关，包括IL-13蛋白（P = 0.04），嗜碱性粒细胞（P = 0.051），嗜酸性粒细胞（P = 0.0018）和总细胞数（P < 0.003）。 BAL中的嗜碱性粒细胞和IL-13水平也具有相关性（P = 0.0002）。结论：这些结果支持了一种免疫调节机制，其中变应原减少了pDC的先天免疫应答和IFN-α的产生，导致变应原暴露部位的炎症和嗜碱性粒细胞因子产生增加。

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