The Essential Role of Single Ig IL-1 Receptor-Related Molecule/Toll IL-1R8 in Regulation of Th2 Immune Response

DOI PDF 被引用文献7件
  • Katarzyna Bulek
    Immunology Department, Lerner Research Institute, Cleveland Clinic Foundation , Cleveland, OH 44195
  • Shadi Swaidani
    Pathobiology Department, Lerner Research Institute, Cleveland Clinic Foundation , Cleveland, OH 44195
  • Jinzhong Qin
    Immunology Department, Lerner Research Institute, Cleveland Clinic Foundation , Cleveland, OH 44195
  • Yi Lu
    Immunology Department, Lerner Research Institute, Cleveland Clinic Foundation , Cleveland, OH 44195
  • Muhammet F Gulen
    Immunology Department, Lerner Research Institute, Cleveland Clinic Foundation , Cleveland, OH 44195
  • Tomasz Herjan
    Immunology Department, Lerner Research Institute, Cleveland Clinic Foundation , Cleveland, OH 44195
  • Booki Min
    Immunology Department, Lerner Research Institute, Cleveland Clinic Foundation , Cleveland, OH 44195
  • Robert A Kastelein
    Schering-Plough Biopharma (formerly DNAX Research) , Palo Alto, CA 94304
  • Mark Aronica
    Pathobiology Department, Lerner Research Institute, Cleveland Clinic Foundation , Cleveland, OH 44195
  • Magdalena Kosz-Vnenchak
    Laboratory of Molecular Genetics and Virology, Department of Biochemistry, Biophysics, and Biotechnology, Jagiellonian University , Krakow,
  • Xiaoxia Li
    Immunology Department, Lerner Research Institute, Cleveland Clinic Foundation , Cleveland, OH 44195

書誌事項

公開日
2009-03-01
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.0802729
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>A novel cytokine IL-33, an IL-1 family member, signals via ST2 receptor and promotes Th2 responses, through the activation of NF-κB and MAP kinases. Previous studies reported that single Ig IL-1R-related molecule (SIGIRR)/Toll IL-1R8 acts as negative regulator for TLR-IL-1R-mediated signaling. We now found that SIGIRR formed a complex with ST2 upon IL-33 stimulation and specifically inhibited IL-33/ST2-mediated signaling in cell culture model. Furthermore, IL-33-induced Th2 response was enhanced in SIGIRR-deficient mice compared with that in wild-type control mice, suggesting a negative regulatory role of SIGIRR in IL-33/ST2 signaling in vivo. Similar to ST2, SIGIRR was highly expressed in in vitro polarized Th2 cells, but not Th1 cells. SIGIRR-deficient Th2 cells produce higher levels of Th2 cytokines, including IL-5, IL-4, and IL-13, than that in wild-type cells. Moreover, SIGIRR-deficient mice developed stronger Th2 immune response in OVA-challenged asthma model. Taken together, our results suggest that SIGIRR plays an important role in the regulation of Th2 response in vivo, possibly through its impact on IL-33-ST2-mediated signaling.</jats:p>

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