Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine that participates in innate and adaptive immune responses. MIF contributes to the resistance against infection agents, but also to the cellular and tissue damage in infectious, autoimmune, and allergic diseases. In the past years, several studies demonstrated a critical role for MIF in the pathogenesis of type-2-mediated inflammation, including allergy and helminth infection. Atopic patients have increased MIF amounts in affected tissues, mainly produced by immune cells such as macrophages, Th2 cells, and eosinophils. Increased MIF mRNA and protein are found in activated Th2 cells, while eosinophils stock pre-formed MIF protein and secrete high amounts of MIF upon stimulation. In mouse models of allergic asthma, the lack of MIF causes an almost complete abrogation of the cardinal signs of the disease including mucus secretion, eosinophilic inflammation, and airway hyper-responsiveness. Additionally, blocking the expression of MIF in animal models leads to significant reduction of pathological signs of eosinophilic inflammation such as rhinitis, atopic dermatitis, eosinophilic esophagitis and helminth infection. A number of studies indicate that MIF is important in the effector phase of type-2 immune responses, while its contribution to Th2 differentiation and IgE production is not consensual. MIF has been found to intervene in different aspects of eosinophil physiology including differentiation, survival, activation, and migration. CD4+ T cells and eosinophils express CD74 and CXCR4, receptors able to signal upon MIF binding. Blockage of these receptors with neutralizing antibodies or small molecule antagonists also succeeds in reducing the signals of inflammation in experimental allergic models. Together, these studies demonstrate an important contribution of MIF on eosinophil biology and in the pathogenesis of allergic diseases and helminth infection.

中文翻译：

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MIF对嗜酸性粒细胞生物学和嗜酸性粒细胞炎症的作用。

巨噬细胞迁移抑制因子（MIF）是一种炎症细胞因子，参与先天性和适应性免疫反应。MIF有助于抵抗感染因子，还有助于感染，自身免疫和过敏性疾病中的细胞和组织损伤。在过去的几年中，几项研究证明了MIF在2型介导的炎症（包括变态反应和蠕虫感染）的发病机理中的关键作用。特应性患者在受影响组织中的MIF含量增加，这主要是由免疫细胞（例如巨噬细胞，Th2细胞和嗜酸性粒细胞）产生的。在活化的Th2细胞中发现MIF mRNA和蛋白增加，而嗜酸性粒细胞则储备了预先形成的MIF蛋白，并在刺激时分泌大量MIF。在过敏性哮喘的小鼠模型中，MIF的缺乏会导致该病的基本体征几乎完全消失，包括粘液分泌，嗜酸性粒细胞炎症和气道高反应性。此外，在动物模型中阻断MIF的表达可导致嗜酸性粒细胞炎症（如鼻炎，特应性皮炎，嗜酸性粒细胞性食管炎和蠕虫感染）的病理征象明显减少。大量研究表明，MIF在2型免疫应答的效应子阶段很重要，而对Th2分化和IgE产生的贡献尚无共识。已经发现MIF干预嗜酸性粒细胞生理学的不同方面，包括分化，存活，激活和迁移。CD4 + T细胞和嗜酸性粒细胞表达CD74和CXCR4受体，它们能够在MIF结合后发出信号。用中和抗体或小分子拮抗剂阻断这些受体也成功减少了实验性过敏模型中的炎症信号。总之，这些研究证明了MIF在嗜酸性粒细胞生物学以及变应性疾病和蠕虫感染的发病机理中的重要贡献。