title: Alteration of immune responses by N-acetylglucosaminyltransferase V during allergic airway inflammation.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  Mgat5-dependent glycosylation of proteins can modulate acquired immune responses, but it is not essential for the development of OVA-induced eosinophilic airway inflammation.
authors.affiliation: Department of Medical Genomics, Graduate School of Frontier Sciences, The University of Tokyo, Japan.
authors.forename: Akiko
authors.initials: A
authors.lastname: Shibui
authors.forename: Aya
authors.initials: A
authors.lastname: Nambu
authors.forename: Eri
authors.initials: E
authors.lastname: Shimura
authors.forename: Sachiko
authors.initials: S
authors.lastname: Yamaguchi
authors.forename: Chiharu
authors.initials: C
authors.lastname: Shiraishi
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Sato
authors.forename: Ko
authors.initials: K
authors.lastname: Okumura
authors.forename: Sumio
authors.initials: S
authors.lastname: Sugano
authors.forename: Nobumichi
authors.initials: N
authors.lastname: Hozumi
authors.forename: Susumu
authors.initials: S
authors.lastname: Nakae
mesh_terms: D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D000939:Epitopes / Q000235:genetics / Q000276:immunology; D006031:Glycosylation; D006967:Hypersensitivity / Q000201:enzymology* / Q000235:genetics / Q000276:immunology*; D007249:Inflammation / Q000201:enzymology / Q000235:genetics / Q000276:immunology; D007962:Leukocytes / Q000276:immunology; D008168:Lung / Q000276:immunology / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D017351:N-Acetylglucosaminyltransferases / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D012140:Respiratory Tract Diseases / Q000201:enzymology* / Q000235:genetics / Q000276:immunology*
chemical_list: D000939:Epitopes; D017351:N-Acetylglucosaminyltransferases