Department of Medicine, Yale University School of Medicine, The Anlyan Center Room S525, New Haven, CT 06520-8031, USA.
J Clin Immunol. 2011 Aug;31(4):666-80. doi: 10.1007/s10875-011-9541-7. Epub 2011 May 11.
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.
我们使用巨噬细胞移动抑制因子（MIF）缺陷小鼠在卵清蛋白经皮致敏模型中研究了巨噬细胞移动抑制因子（MIF）在 Th2 反应产生中的作用。与野生型相比，经抗原刺激后，致敏的 MIF 缺陷小鼠的淋巴结细胞产生的 Th2 细胞因子水平较低。经鼻暴露于抗原后，缺乏 MIF 的致敏小鼠肺部炎症较少。缺乏 MIF 受体 CD74 的小鼠也无法对经皮致敏产生炎症反应。使用 DO11.10 OVA TCR 转基因动物检查特应性反应的激发阶段，结果表明，MIF 缺陷型 T 细胞的 T 细胞增殖和 IL-2 产生受到严重抑制。当 T 细胞和抗原呈递细胞均缺乏 MIF 时，这种缺陷最为明显。这些数据表明，MIF 对于过敏性疾病中 Th2 型免疫反应的致敏和激发阶段都是至关重要的。
