IFN-γ Secreted by CD103+ Dendritic Cells Leads to IgG Generation in the Mesenteric Lymph Node in the Absence of Vitamin A

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  • Jae-Hoon Chang
    *Mucosal Immunology Section, International Vaccine Institute, Seoul, South Korea 151-818; and
  • Hye-Ran Cha
    *Mucosal Immunology Section, International Vaccine Institute, Seoul, South Korea 151-818; and
  • Sun-Young Chang
    *Mucosal Immunology Section, International Vaccine Institute, Seoul, South Korea 151-818; and
  • Hyun-Jeong Ko
    *Mucosal Immunology Section, International Vaccine Institute, Seoul, South Korea 151-818; and
  • Sang-Uk Seo
    *Mucosal Immunology Section, International Vaccine Institute, Seoul, South Korea 151-818; and
  • Mi-Na Kweon
    *Mucosal Immunology Section, International Vaccine Institute, Seoul, South Korea 151-818; and

説明

<jats:title>Abstract</jats:title> <jats:p>Although the induction mechanism of secretory IgA has been well studied, that of IgG in the mucosal compartments is not well understood. In this study, vitamin A deficiency was convincingly shown to be associated with increased IgG in serum and intestinal fluid. We found increased numbers of IgG-secreting B cells in the lamina propria of the small intestine and mesenteric lymph node (MLN) of vitamin A-deficient (VAD) mice. Of note, IFN-γ secreted by MLN dendritic cells (DCs) was significantly augmented in VAD mice, unlike control mice, and CD103+ DCs were the main subsets to secrete IFN-γ. The aberrant increase of IgG in VAD mice can be ascribable to IFN-γ, because IFN-γ−/− VAD mice have normal IgG levels and the addition of rIFN-γ increased IgG production by B cells cocultured with MLN DCs from IFN-γ−/− VAD mice. Oral feeding of antibiotics resulted in significant reduction of IgG in VAD mice, indicating a critical role for altered commensal bacteria for IgG class-switching recombination in the absence of vitamin A. Collectively, vitamin A deficiency provokes the generation of IFN-γ–secreting CD103+ DCs, which may be a critical regulator for IgG generation in the MLN.</jats:p>

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