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. 2018 Sep 3;215(9):2445–2461. doi: 10.1084/jem.20180230

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© 2018 Wray-Dutra et al.

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Figure 3. — GC B cell–intrinsic aCARD11 expression induces rapid GC peak and contraction with increased terminal differentiation. (A) Left: GFP expression in Ctrl (Cre-negative littermates) and aCard11^+/+ mice crossed with the Cγ1-Cre strain showing non-GC (B220⁺CD95^loCD38^hi) and GC (B220⁺CD95^hiCD38^lo) B cells at 5 d postimmunization (dpi) with SRBCs. Filled histogram: non-GC (gray, Ctrl; pink, Cγ1-aCard11); open histogram: GC (black, Ctrl; red, Cγ1-aCard11). Right: GFP expression in PCs (B220⁻CD138⁺). (B) Percentage of splenic GC B cells in PBS controls and at 5 and 7 dpi with SRBC (P = 0.001 at 7 dpi). (C) Percentage of splenic PCs after immunization (P < 0.001 at 7 dpi). To measure antigen-specific antibody response, Cγ1-aCard11^+/− and control mice (Cre-negative littermates and Cγ1^Cre/+) were injected with PBS or 50 μg NP-CGG injected i.p. For B and C, significance was calculated by two-way ANOVA. Data represent six Ctrl mice, four Cγ1-aCard11 PBS-injected mice; SRBC injected, day 5: six Ctrl mice, six Cγ1-aCard11 (three expts) mice; day 7: 16 Ctrl mice, 12 Cγ1-aCard11 (6 expts) mice. (D) Low- (NP-30; P = 0.006) and high-affinity (NP-5; P = 0.0006) NP-specific IgG serum titers. (E) Low- (P < 0.0001) and high-affinity (P = 0.0001) NP-specific IgG1 serum titers. (D and E) Significance calculated by one-way ANOVA. Data are representative of 33 Ctrl mice and 21 Cγ1-aCard11^+/− mice 12 dpi with NP-CGG from seven independent experiments. For summary graphs, lines and error bars represent mean ± SEM. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.