Fig. 7: SCFAs inhibit AICDA/Aicda and PRDM1/Prdm1 expression, CSR, and plasma cell differentiation through their HDAC inhibitory activity.

a, b Human and mouse B cells were stimulated with CD154 plus IL-4 and IL-21, or CD154 plus IL-4, respectively, in the presence of nil, butyrate (500 μM), propionate (2000 μM), butyrate (500 μM) plus propionate (2000 μM) alone, or butyrate (2000 μM) plus propionate (2000 μM) together with increasing doses of GPR43 inhibitor GLPG0974. Human B cell AICDA and PRDM1 transcripts as well as mouse B cell Aicda and Prdm1 transcripts were analyzed 72 h post stimulation by qRT-PCR and normalized to HRPT and Gapdh expression, respectively. Data are ratios to stimulated B cells cultured with nil (set as 1; means ± SEM of three independent experiments) (a). Proportion of CD19⁺IgG⁺ B cells were analyzed 120 h post stimulation by flow cytometry. Data are representative of three independent experiments yielding comparable results (b). c–f Mouse B cells were stimulated with LPS plus IL-4, in the presence of increasing doses of butyrate, propionate, palmitate, and SAHA. Expression of Aicda and Prdm1 transcripts were analyzed 72 h post stimulation by qRT-PCR and normalized to Gapdh expression. Data are ratios to stimulated B cells cultured with nil (set as 1; means ± SEM of three independent experiments) (c). The proportion of CD19⁺ IgG1⁺ B cells and CD138⁺ plasmablasts/plasma cells were analyzed 120 h post stimulation by flow cytometry. Data are representative of three independent experiments yielding comparable results (d–f). *p < 0.05, **p < 0.01, ***p < 0.001 (unpaired t test). The source data are provided in Source Data file.