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. 2018 Dec 20;3(24):e124646. doi: 10.1172/jci.insight.124646

Figure 2. Recipient C3 deficiency prevents GC B cell formation and autoantibody production in a model of parent→F1 alloimmunity.

Figure 2

CD8-depleted WT B6 spleen cells were injected i.v. into WT or C3–/– (bxd)F1 recipients and analyses were performed on day 14. (A) Representative histograms depicting percentages of host-derived (H-2Kd+B220+) Fas+GL7+ GC B cells (top) and IgM–IgD– class-switched B cells (bottom) in naive (bxd)F1 (left), WT (bxd)F1 (middle), and C3–/– (bxd)F1 (right) recipients. (B) Total numbers of host-derived B220+Fas+GL7+ cells and IgM–IgD– class-switched B cells in day 14 spleens of naive (bxd)F1 (no cell transfer) and in WT (bxd) and C3–/– (bxd)F1 recipients. (C) Anti-dsDNA autoantibodies (AU/ml) in sera collected from naive (bxd)F1 mice or WT (bxd) and C3–/– (bxd)F1 recipients on day 14. Combined data of 2 separate experiments (6–7 mice per group). **P < 0.01, ***P < 0.001 by Student’s t test.