Role of Macrophage Migration Inhibitory Factor in the Th2 Immune Response to Epicutaneous Sensitization
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  • 作者：Rituparna Das (1)
    Jeremy E. Moss (2)
    Eve Robinson (23)
    Scott Roberts (1)
    Rebecca Levy (1)
    Yuka Mizue (1)
    Lin Leng (1)
    Courtney McDonald (1)
    Robert E. Tigelaar (23)
    Christina A. Herrick (23)
    Richard Bucala (1) richard.bucala@yale.edu
  • 关键词：Atopic inflammation – ; macrophage migration inhibitory factor – ; Th2 response
  • 刊名：Journal of Clinical Immunology
  • 出版年：2011
  • 出版时间：August 2011
  • 年：2011
  • 卷：31
  • 期：4
  • 页码：666-680
  • 全文大小：3.5 MB
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  • 作者单位：1. Department of Medicine, Yale University School of Medicine, The Anlyan Center Room S525, 300 Cedar Street, New Haven, CT 06520-8031, USA2. Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA3. Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
  • 刊物类别：Biomedical and Life Sciences
  • 刊物主题：Biomedicine
    Immunology
    Infectious Diseases
    Internal Medicine
    Medical Microbiology
  • 出版者：Springer Netherlands
  • ISSN：1573-2592
文摘
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.

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