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

Title
IFN-gamma Secreted by CD103(+) Dendritic Cells Leads to IgG Generation in the Mesenteric Lymph Node in the Absence of Vitamin A
Author(s)
장재훈Hye-Ran Cha[Hye-Ran Cha]Sun-Young Chang[Sun-Young Chang]Hyun-Jeong Ko[Hyun-Jeong Ko]Sang-Uk Seo[Sang-Uk Seo]Mi-Na Kweon[Mi-Na Kweon]
Keywords
INFLAMMATORY-BOWEL-DISEASE; NEONATAL FC-RECEPTOR; RETINOIC ACID; SMALL-INTESTINE; DEFICIENT MICE; LAMINA PROPRIA; B-CELLS; RESPONSES; ANTIBODIES; BACTERIA
Issue Date
201106
Publisher
AMER ASSOC IMMUNOLOGISTS
Citation
JOURNAL OF IMMUNOLOGY, v.186, no.12, pp.6999 - 7005
Abstract
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-gamma 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-gamma. The aberrant increase of IgG in VAD mice can be ascribable to IFN-gamma, because IFN-gamma(-/-) VAD mice have normal IgG levels and the addition of rIFN-gamma increased IgG production by B cells cocultured with MLN DCs from IFN-gamma(-/-) 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-gamma-secreting CD103(+) DCs, which may be a critical regulator for IgG generation in the MLN. The Journal of Immunology, 2011, 186: 6999-7005.
URI
http://hdl.handle.net/YU.REPOSITORY/25135http://dx.doi.org/10.4049/jimmunol.1003484
ISSN
0022-1767
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약학대학 > 약학부 > Articles
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