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. 2016 May 2;213(5):733–750. doi: 10.1084/jem.20151724

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© 2016 Jackson et al.

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Figure 4. — B cell–intrinsic IFN-γR signals promote spontaneous autoimmune GCs. (A) Number of IFN-γ⁺CD4⁺ T cells in WT, Was^−/−, and B cell–intrinsic Tlr7^−/−, Tlr9^−/−, and MhcII^−/− chimeras. (B) Anti-dsDNA and anti-Sm/RNP IgM, IgG, and IgG2c auto-Abs (12 wk after transplantation) in WT and Was^−/− chimeras as well as Was^−/− chimeras with global or B cell–intrinsic deletion of IFN-γR. (C) Spleen weight. (D) Number of splenic CD4⁺ T cells, CD11b⁺GR1^lo monocyte/macrophages, and CD11b⁺GR1⁺ neutrophils. (E and F) Representative FACS plots (E; gated on CD19⁺) and percentage (F) of splenic PNA⁺FAS⁺ GC B cells. (G) Representative splenic sections stained with B220, PNA, and CD3. Bars, 100 µm. (H and I) Representative FACS plots (H; gated on CD4⁺) and number (I) of splenic PD1⁺CXCR5⁺ Tfh cells. (J) Number of naive (CD44^LOCD62L^HI) and EM (CD44^HICD62L^LO/HI) CD4⁺ T cells. (K) Total serum IgM, IgG, IgG2b, and IgG2c titers in the indicated chimeras. Data are representative of five WT (n = 10), five Was^−/− (n = 18), two global Ifngr^−/− Was^−/− (n = 10), and four B cell–intrinsic Ifngr^−/− Was^−/− (n = 13) chimeras, as well as three Was^−/−.Tlr7^−/− (n = 14), three Was^−/−.Tlr9^−/− (n = 15), and two Was^−/−.MhcII^−/− (n = 8) chimeras sacrificed at 24 wk after transplantation. Error bars indicate SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001, by the Kruskal-Wallis one-way ANOVA.