Constitutive genetic depletion of CD11c ⁺ B cells improves renal disease and reduces T cell activation (A) Mixed bone marrow chimeras were generated in J_H^−/− MRL/lpr recipients with indicated bone marrow. Data are pooled from three independently generated cohorts of chimeras. (B–S) Recipients were assessed at 24 wk after chimerism for (B) spleen weight; (C) spleen cell number; proportion of (D) CD11c⁺MHCII⁺ conventional dendritic cells of live, (E) CD317⁺ SiglecH⁺ plasmacytoid dendritic cells of live, (F) TCRβ⁺ T cells of live, (G) CD19⁺ B cells of live, (H) CD11c⁻ CD11b⁺ ABCs among B cells, (I) CD11c⁺CD11b⁺ ABCs among B cells, (J) CD11c⁺CD11b⁻ ABCs among B cells, (K) CD44⁺ CD138⁺ PBs among B cells. (L–M) H&E-stained kidney sections were assessed for (L) interstitial infiltrates and (M) glomerulonephritis. (N) Urine was assessed for proteinuria by albustix. (O and P) Frequency of CD44^lowCD62L⁺ (naive) cells among (O) CD4 T cells or (P) CD8 T cells. (Q) anti-nucleosome IgG, (R) anti-nucleosome IgG2a, and (S) anti-RNA IgG were measured by ELISA. Statistical comparisons by one-tailed Mann-Whitney; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.