Lithocholic acid controls adaptive immune responses by inhibition of Th1 activation through the Vitamin D receptor
Fig 2
LCA inhibits CD4+ Th cell activation.
(A) IFNγ mRNA expression and (B) TNFα mRNA expression in Jurkat T cells in response to 10 μM LCA treatment (light grey lines) or vehicle (dark grey lines) with P/I activation (triangles) or in resting Jurkat T cells (squares). (C) IFNγ and (D) TNFα mRNA expression in P/I-activated Jurkat T cells in response to increasing concentrations of LCA. (E) Secreted TNFα protein levels of Jurkat T cells in the supernatant in response to 10 μM LCA treatment (light grey lines) or vehicle (dark grey lines) with P/I activation (triangles) or in resting Jurkat T cells (squares). (F) mRNA expression of IFNγ, IL-6, CD40L, TNFα in primary mouse CD4+ Th cells activated with P/I and treated with 10 μμM LCA (light grey bars) or vehicle (dark grey bars). (G) mRNA expression of IFNγ, IL-6, CD40L, TNFα in primary human CD4+ Th cells stimulated with Dynabeads T-activator (T-act) and treated with 10 μM LCA (light grey bars) or vehicle (dark grey bars). P/I, PMA/ionomycin; LCA, lithocholic acid; AU, Arbitrary units. Results represent the mean ± SEM. *Statistically significant, P<0.05. Experiments were performed in triplicates and repeated at least twice.