Role of Macrophage Migration Inhibitory Factor in the Th2 Immune Response to Epicutaneous Sensitization
Role of Macrophage Migration Inhibitory Factor in the Th2 Immune Response to Epicutaneous Sensitization
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DOI：
10.1007/s10875-011-9541-7
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发表时间：
2011-08-01
影响因子：
9.1
通讯作者：
Bucala, Richard
中科院分区：
文献类型：
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作者：
Das, Rituparna;Moss, Jeremy E.;Bucala, Richard
我们研究了巨噬细胞移动抑制因子(MIF)在利用MIF缺陷小鼠产生Th2反应中的作用，该模型采用皮肤表面致敏卵蛋白的模型。与野生型相比，致敏MIF缺陷小鼠的淋巴结细胞在抗原攻击后产生较低水平的Th2细胞因子。缺乏MIF的致敏小鼠在鼻腔暴露抗原后肺部炎症较少。缺乏MIF受体CD74的小鼠也无法对皮肤表面致敏产生炎症反应。使用DO11.10 OVA TCR转基因动物对特应性反应的激发阶段的检测表明，MIF缺陷的T细胞的T细胞增殖和IL-2的产生严重受损。当T细胞和抗原提呈细胞都缺乏MIF时，这种缺陷最为严重。这些数据表明，在过敏性疾病中，MIF对于Th2型免疫反应的敏化和诱导阶段都是至关重要的。
We examined the role of macrophage migration inhibitory factor (MIF) in the generation of the Th2 response using MIF-deficient mice in a model of epicutaneous sensitization to ovalbumin. Lymph node cells from sensitized MIF-deficient mice produce lower levels of Th2 cytokines after antigen challenge when compared to their wild-type counterparts. Sensitized mice lacking MIF show less pulmonary inflammation after intranasal antigen exposure. Mice deficient in CD74, the MIF receptor, also are unable to generate an inflammatory response to epicutaneous sensitization. Examination of the elicitation phase of the atopic response using DO11.10 OVA TCR transgenic animals shows that T cell proliferation and IL-2 production are strongly impaired in MIF-deficient T cells. This defect is most profound when both T cells and antigen-presenting cells are lacking MIF. These data suggest that MIF is crucial both for the sensitization and the elicitation phases of a Th2-type immune response in allergic disease.