Abstract
Retinoic acid (RA) is a critical regulator of the intestinal adaptive immune response. However, the intrinsic impact of RA on B cell differentiation in the regulation of gut humoral immunity in vivo has never been directly shown. To address this issue, we have been able to generate a mouse model where B cells specifically express a dominant-negative receptor α for RA. In this study, we show that the silencing of RA signaling in B cells reduces the numbers of IgA(+) Ab-secreting cells both in vitro and in vivo, suggesting that RA has a direct effect on IgA plasma cell differentiation. Moreover, the lack of RA signaling in B cells abrogates Ag-specific IgA responses after oral immunization and affects the microbiota composition. In conclusion, these results suggest that RA signaling in B cells through the RA receptor α is important to generate an effective gut humoral response and to maintain a normal microbiota composition.
Original language | English |
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Pages (from-to) | 1368-1371 |
Number of pages | 4 |
Journal | Journal of Immunology |
Volume | 195 |
Issue number | 4 |
DOIs | |
Publication status | Published - 15 Aug 2015 |
Keywords
- Animals
- B-Lymphocytes
- Cell Differentiation
- Gastrointestinal Tract
- Gene Expression
- Immunization
- Immunoglobulin A
- Mice
- Mice, Transgenic
- Microbiota
- Plasma Cells
- Receptors, Retinoic Acid
- Signal Transduction
- Tretinoin