title: Intravenous IgA complexed with antigen reduces primary antibody response to the antigen and anaphylaxis upon antigen re-exposure by inhibiting Th1 and Th2 activation in mice.
abstract: BACKGROUND
  Serum IgG, IgE and IgM have been shown to enhance the primary antibody responses upon exposure to the soluble antigens recognized by those antibodies. However, how IgA affects these responses remains unknown.
  
  
  OBJECTIVE
  We investigated the effects of intravenously administered monoclonal IgA on the immune responses in mice.
  
  
  METHODS
  DBA/1J mice were immunized with ovalbumin in the presence or absence of anti-ovalbumin monoclonal IgA. The Th1 and Th2 immune responses to ovalbumin and the anaphylaxis induced by re-exposure to ovalbumin were measured.
  
  
  RESULTS
  IgA complexed with antigen attenuated the primary antibody responses to the antigen in mice, in contrast to IgG2b and IgE. The primary antibody responses, i.e. the de novo synthesis of anti-ovalbumin IgG2a, IgG1 and IgE in the serum, and the subsequent anaphylaxis induced with re-exposure to ovalbumin were reduced by the co-injection of anti-ovalbumin monoclonal IgA at ovalbumin immunization. The Th1, Th2 and Tr1 cytokines interferon-γ, interleukin-4 and interleukin-10, respectively, released from ovalbumin-restimulated cultured splenocytes collected from allergic mice were also reduced by the treatment. The induction of interferon-γ and interleukin-4 secretion by splenocytes from ovalbumin-immunized mice stimulated in vitro with ovalbumin was also significantly reduced by the antigen complexed with anti-ovalbumin IgA.
  
  
  CONCLUSIONS
  These data suggest that the direct inhibition of Th1 and Th2 activation by anti-ovalbumin monoclonal IgA participates in the inhibition of the primary antibody responses. IgA plays important immunosuppressive roles under physiological and pathological conditions and is a promising candidate drug for the treatment of immune disorders.
authors: Department of Pharmacology, Kobe Pharmaceutical University , Kobe, Hyogo , Japan.
authors: Kouya
authors: K
authors: Yamaki
authors: Kenji
authors: K
authors: Miyatake
authors: Takayuki
authors: T
authors: Nakashima
authors: Ayumi
authors: A
authors: Morioka
authors: Midori
authors: M
authors: Yamamoto
authors: Yuki
authors: Y
authors: Ishibashi
authors: Ayaka
authors: A
authors: Ito
authors: Ayu
authors: A
authors: Kuranishi
authors: Shin
authors: S
authors: Yoshino
mesh_terms: D000707:Anaphylaxis / Q000517:prevention & control*; D000818:Animals; D000917:Antibody Formation / Q000187:drug effects*; D000936:Antigen-Antibody Complex / Q000008:administration & dosage / Q000494:pharmacology*; D002478:Cells, Cultured; D000939:Epitopes / Q000276:immunology; D005260:Female; D007070:Immunoglobulin A / Q000008:administration & dosage / Q000494:pharmacology*; D016756:Immunoglobulins, Intravenous / Q000008:administration & dosage / Q000494:pharmacology*; D008213:Lymphocyte Activation / Q000187:drug effects; D051379:Mice; D008811:Mice, Inbred DBA; D010047:Ovalbumin / Q000276:immunology; D018417:Th1 Cells / Q000187:drug effects / Q000276:immunology*; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology*
chemical_list: D000936:Antigen-Antibody Complex; D000939:Epitopes; D007070:Immunoglobulin A; D016756:Immunoglobulins, Intravenous; D010047:Ovalbumin
keywords: Anaphylaxis; IgA; Th1/Th2; immunosuppression; primary antibody response