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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 publication




Journal article


Journal of immunology (Baltimore, Md. : 1950)

Publication Date





1368 - 1371


Department of Immune Regulation and Intervention, Division of Transplantation Immunology and Mucosal Biology, Guy's Hospital, King's College London, London SE1 9RT, United Kingdom;


Gastrointestinal Tract, B-Lymphocytes, Plasma Cells, Animals, Mice, Transgenic, Mice, Tretinoin, Immunoglobulin A, Receptors, Retinoic Acid, Immunization, Signal Transduction, Cell Differentiation, Gene Expression, Microbiota