IL-4 exacerbates anaphylaxis
IL-4 exacerbates anaphylaxis
复制标题
DOI：
10.4049/jimmunol.170.7.3835
复制
发表时间：
2003-04-01
影响因子：
4.4
通讯作者：
Finkelman, FD
中科院分区：
文献类型：
--
作者：
Strait, RT;Morris, SC;Finkelman, FD
我们评估了IL-4（一种诱导过敏反应的关键细胞因子）是否也参与了过敏的效应期：用IL-4或相关细胞因子IL-13预处理小鼠，可迅速显著增加由交联Fc ε RI或Fc γ RIII诱导的过敏反应的严重程度。这种作用被内源性产生的IFN-γ抑制，是T细胞、B细胞和共同γ链非依赖性的，并且需要IL-4 R α和Stat 6。IL-4 R α信号也增强了感染线虫寄生虫的小鼠的过敏反应，该线虫寄生虫刺激IL-4/IL-13的产生。IL-4通过与血管活性介质协同作用增加血管通透性而加重过敏反应。在变应性炎症的效应阶段，IL-4和血管活性介质之间的协同作用可能既有助于变应性免疫病理学，又增强对胃肠道蠕虫的保护性免疫。
We evaluated whether IL-4, a cytokine critical for inducing allergic responses, also contributes to the effector phase of allergy: Pretreatment of mice with IL-4 or the related cytokine, IL-13, rapidly and dramatically increased the severity of anaphylaxis induced by cross-linking FcepsilonRI or FcgammaRIII. This effect was inhibited by endogenously produced IFN-gamma, was T cell-, B cell-, and common gamma-chain-independent, and required IL-4Ralpha and Stat6. IL-4Ralpha signaling also enhanced anaphylaxis in mice infected with a nematode parasite that stimulates IL-4/IL-13 production. IL-4 exacerbated anaphylaxis by acting synergistically with vasoactive mediators to increase vascular permeability. Synergy between IL-4 and vasoactive mediators during the effector phase of allergic inflammation may both contribute to allergic immunopathology and enhance protective immunity against gastrointestinal worms.