Skip to main content
. Author manuscript; available in PMC: 2022 Nov 1.
Published in final edited form as: J Immunol. 2021 Sep 29;207(9):2217–2222. doi: 10.4049/jimmunol.2100548

Figure 3: Distinct EF and GC-dependent pathways contribute to lupus autoAb.

Figure 3:

(A, B) Anti-dsDNA IgG (A) and Ig subclass amongst DNA-reactive samples (B) in global Cd28−/− WAS model. (C) Serum IgG2c autoAb by autoantigen microarray. Each column represents pooled sera from an independent chimera cohort. (D, E) Serum anti-dsDNA (D) and anti-Sm/RNP (E) autoAb. (F) Splenic sections stained with B220 (red), IgG2c (green) and CD3 (blue), showing expansion of IgG2c+ foci in splenic red pulp in WAS and B cell Cd80/Cd86-deficient WAS chimeras, but not Cd28−/− chimeras; bars, 100μm. (G) Splenic B220loCD138+ plasma cell number. (H) SHM analysis: mutation count in κ light chains from sorted splenic B220loCD138+ plasma cells. (I) CD11b+CD11c+ ABCs (% of CD19+ B cells). (A,B,D,E,G,H,I) *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001; NS, not-significant; by one-way ANOVA and Tukey’s multiple comparison test (A,D,E,G,I), and by two-tailed Student’s t test (B, H). Each data point equals individual animal.