| First Author | Chang JH | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 12 | Pages | 6999-7005 |
| PubMed ID | 21572021 | Mgi Jnum | J:175489 |
| Mgi Id | MGI:5285798 | Doi | 10.4049/jimmunol.1003484 |
| Citation | Chang JH, et al. (2011) IFN-gamma secreted by CD103+ dendritic cells leads to IgG generation in the mesenteric lymph node in the absence of vitamin A. J Immunol 186(12):6999-7005 |
| abstractText | 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. |
