The kidneys of NZB/B1, NZO/B1, NZC/B1 and NZY/B1 mice

Role of perforin in controlling B-cell hyperactivity and humoral autoimmunity

“…Proteinuria in acute GVHD did not differ significantly from control mice (=1+). Low-level proteinuria seen in control mice (=1+) has been previously reported in normal mice and is not indicative of glomerular disease (23), as confirmed in Figure 5a. The foregoing data demonstrate that, although the onset of GVHD in B6pfp→F1 mice resembles acute GVHD (B6wt→F1), incomplete elimination of activated autoreactive B cells in B6pfp→F1 mice results in persistent humoral autoimmunity and conversion of disease phenotype to that of chronic GVHD.…”

“…The number of host B cells did not differ significantly between the two groups (data not shown), thus the greater amounts of anti-ssDNA in chronic GVHD mice likely reflects the greater number of donor CD4 + T cells that persists in chronic GVHD compared with pfp GVHD mice ( Table 2 Glomerulonephritis in pfp GVHD mice. To determine whether pfp GVHD mice developed a lupuslike glomerulonephritis similar to that reported in chronic GVHD mice (22,23), renal function and pathological analysis of the kidneys were performed. Increased proteinuria (≥ 2+) was seen for both pfp→F1 and chronic GVHD mice at 4 weeks (pfp GVHD or chronic GVHD vs. control P < 0.001; n = 8-9 per group) and at 11 weeks (pfp GVHD or chronic GVHD vs. control P < 0.01; n = 4 per group) after disease induction.…”