Skip to main content
. Author manuscript; available in PMC: 2015 Apr 15.
Published in final edited form as: J Immunol. 2014 Mar 19;192(8):3607–3617. doi: 10.4049/jimmunol.1301284

Figure 4.

Figure 4

B cell antigen presentation preferentially drives TFH differentiation in response to viral infection. B-MHCII and MHCII KO mice received 1×107 CD4+ T cells from C57/BL6 mice 7–14 days prior to infection to reconstitute the CD4+ T cell compartment. 1×104 SMARTA transgenic CD4+ T cells were transferred to WT and B-MHCII mice and the mice were infected with LCMV Armstrong one day later. Splenocytes were analyzed on day 8 post infection. (A) Representative FACS plots of CD19 TCRβ+ CD4+ SMARTA cells to identify CXCR5+ PD-1+ TFH cells. (B) Percentage of SMARTA cells in WT and B-MHCII mice that are CXCR5+ PD-1+ TFH cells. (C) Total number of splenic SMARTA TFH cells in WT, B-MHCII and MHCII KO mice. (D) Histogram overlay of Bcl6 expression by CXCR5+ PD-1+ SMARTA TFH cells. (E) Relative expression of IL-21 mRNA in sorted CXCR5+ PD-1+ SMARTA cells. (F) Total number of CD19= B220+ IgDlo GL-7+ GC B cells. (G) Measurement of LCMV specific IgG in the serum on d8 p.i., compared to uninfected C57/BL6 mice. * denotes a p value of < 0.05, ** denotes a p value of <0.01 and *** denotes a p value of <0.001 calculated using Student’s t test. Bar graphs show mean ± SEM. Data are representative of 2 independent experiments with 3–6 mice per group.