Immune responses to Aspergillus antigen in IL-4-/-mice and the effect of eosinophil ablation.
Immune responses to Aspergillus antigen in IL-4-/-mice and the effect of eosinophil ablation.
复制标题
IL-4-/-小鼠对曲霉菌抗原的免疫反应和嗜酸性粒细胞消融的作用。
DOI：
10.1034/j.1398-9995.1999.00944.x
复制
发表时间：
1999
期刊：
影响因子：
12.4
通讯作者：
Fink,JN
中科院分区：
文献类型：
--
作者：
Kurup,VP;Choi,HY;Murali,PS;Xia,JQ;Coffman,RL;Fink,JN
背景：暴露于烟曲霉过敏原导致小鼠血清总IgE和外周血嗜酸性粒细胞升高。相关的肺部炎症和免疫反应与人类过敏性支气管肺曲菌病的检测结果相当。过敏原诱导的细胞因子被认为调节这些动物的炎症和免疫反应。方法：本研究将C57BL/6和BALB/c小鼠暴露于a。fumigatusantigen。这两种菌株的动物表型均为野生型和IL - 4敲除型。一些动物也接受抗IL - 5或抗IFN - γ治疗。研究了血清总IgE、曲霉菌种IgG亚类、外周血嗜酸性粒细胞和肺组织学。结果：结果显示，暴露于a的所有野生型和IL - 4 - / -动物的肺部炎症相似。fumigatusantigen。同样，尽管抗细胞因子治疗产生了不同的免疫反应，但在研究的任何动物组中都没有发现重大差异。结论：可以得出结论。在免疫未改变的宿主中，烟曲霉暴露主要是Th2型，并且Th2细胞因子的消耗导致类似的肺部炎症，但具有特征性的Th1反应，这表明过敏性曲霉病的发病机制是多种诱导途径的结果。
Background: Exposure toAspergillus fumigatusallergens results in enhanced total serum IgE and peripheral blood eosinophils in mice. The associated pulmonary inflammation and immunologic responses are comparable to those detected in human allergic bronchopulmonary aspergillosis. Allergen‐induced cytokines are thought to regulate the inflammatory and immune responses in these animals.Methods: In the present study, we exposed C57BL/6 and BALB/c mice toA. fumigatusantigen. Both wild‐type and IL‐4 knockout phenotypes of animals of both strains were used. Some animals were also treated with anti‐IL‐5 or anti‐IFN‐γ. Total serum IgE,Aspergillusspecies IgG subclass, peripheral blood eosinophils, and lung histology were studied.Results: The results demonstrate similar lung inflammation in all wild‐type and IL‐4‐/‐ animals exposed toA. fumigatusantigen. Similarly, in spite of the diverse immune response produced by the anticytokine treatment, no major differences were detected among any of the animal groups studied.Conclusions: It can be concluded thatA. fumigatusexposure in an immunologically unaltered host is predominantly of a Th2 type, and that depletion of the Th2 cytokine leads to a similar lung inflammation but with a characteristic Th1 response, suggesting that the pathogenesis of allergic aspergillosis is the result of multiple induction pathways.