Alteration of Immune Responses by N-acetylglucosaminyltransferase V during Allergic Airway Inflammation

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Author(s)

    • Shibui Akiko
    • Department of Medical Genomics, Graduate School of Frontier Sciences, The University of Tokyo|Research Institute for Biological Sciences, Tokyo University of Science
    • Nakae Susumu
    • Frontier Research Initiative, The Institute of Medical Science, The University of Tokyo|Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo
    • Nambu Aya
    • Atopy Research Center, Juntendo University|Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo
    • Yamaguchi Sachiko
    • Frontier Research Initiative, The Institute of Medical Science, The University of Tokyo
    • Sato Yoshitaka
    • Research Institute for Biological Sciences, Tokyo University of Science
    • Sugano Sumio
    • Department of Medical Genomics, Graduate School of Frontier Sciences, The University of Tokyo
    • Hozumi Nobumichi
    • Research Institute for Biological Sciences, Tokyo University of Science|Faculty of Health Sciences, Ryotokuji University

Abstract

<b>Background:</b> β-1,6-N-acetylglucosaminyltransferase V (Mgat5 or GlcNac-TV), which is involved in the glycosylation of proteins, is known to be important for down-regulation of TCR-mediated T-cell activation and negatively regulates induction of contact dermatitis and experimental autoimmune encephalomyelitis. However, the role of Mgat5 in the induction of allergic airway inflammation remains unclear.<br> <b>Methods:</b> To elucidate the role of Mgat5 in the pathogenesis of allergic airway inflammation, ovalbumin (OVA)-induced airway inflammation was induced in Mgat5-deficient mice. The OVA-specific lymphocyte proliferation and cytokine production levels, OVA-specific IgG1, IgG2a and IgE levels in the serum, and the number of leukocytes and cytokine levels in the bronchoalveolar lavage (BAL) fluid were compared between wild-type and Mgat5-deficient mice.<br> <b>Results:</b> OVA-specific lymphocyte proliferation and production of IFN-γ and IL-10, but not IL-4, were increased in Mgat5-deficient mice, suggesting that Th2-type immune responses are seemed to be suppressed by increased IFN-γ and IL-10 production in these mice. However, Th2-type responses such as OVA-specific IgG1, but not IgE, and IL-5 levels in BAL fluids were increased in Mgat5-deficient mice. Meanwhile, the number of eosinophils was normal, but the numbers of neutrophils, macrophages and lymphocytes were reduced, in these mutant mice during OVA-induced airway inflammation.<br> <b>Conclusions:</b> Mgat5-dependent glycosylation of proteins can modulate acquired immune responses, but it is not essential for the development of OVA-induced eosinophilic airway inflammation.<br>

Journal

  • Allergology International

    Allergology International 60(3), 345-354, 2011

    Japanese Society of Allergology

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