Background <p>Peripheral helper T cells represent a recently characterized subset of CD4⁺ T cells present in inflammatory bowel disease (IBD) patients. Bile acids act as signaling molecules in immune regulation. However, the role of bile acids in Tph cell differentiation remains unclear.</p> Methods <p>Immunofluorescence staining was used to detect the presence of Tph cells in intestinal tissue samples; Wild-type (WT) and <i>Fxr</i>^{<i>−/−</i>} mice were treated with or without the FXR agonist obeticholic acid (OCA) in dextran sulfate sodium (DSS)-induced acute colitis. The proportions of Tph cells and innate immune cells were analyzed by FACS. Bone marrow-derived dendritic cells (BMDCs) and naïve T cells of WT and <i>Fxr</i>^{<i>−/−</i>} mice were sorted, differentiated and cultured in vitro to observe the regulatory effects of FXR on BMDCs function and Tph cell differentiation.</p> Results <p>Tph proportion was significantly elevated in inflamed intestinal tissues. OCA treatment increased the Tph cell proportion in the intestinal LP of WT mice. The proportion of dendritic cells (DCs) in the LP of <i>Fxr</i>^{<i>−/−</i>} mice was significantly lower than WT mice after DSS-mediated colitis induction. FXR deficiency impaired the ability of BMDCs to induce Tph cell differentiation in vitro. CD11c and MHC-II expression levels were reduced in BMDCs from <i>Fxr</i>^{<i>−/−</i>} mice upon stimulation with LPS. FXR deficiency activated the PPAR-γ signaling pathway and decreased IL-12 expression in BMDCs.</p> Conclusion <p>Tph cell levels were elevated in inflamed intestinal tissues. FXR suppression in BMDCs was associated with activated PPAR-γ signaling; and with reduced DC maturation, IL-12 secretion, and Tph cell differentiation.</p> Graphical abstract <p></p>