Fig. 2
From: Pathogenic role of glycan-specific IgG antibodies in IgA nephropathy
The biological effect of IgG-ddIgA1 complexes on cultured human mesangial cells. IgG-ddIgA1 complexes from both patients with IgA nephropathy (IgAN-IgG-ddIgA1) and healthy controls (IgAN-IgG-ddIgA1) could induce mesangial cells proliferation (a) and up-regulated excretion of MCP-1 (b), IL-6 (c) and CXCL1 (d). The levels of mesangial cells proliferation induced by IgAN-IgG-dd-IgA1 were significantly higher than those induced by HC-IgG-dd-IgA1 (1.10 ± 0.05 vs. 1.03 ± 0.03; p < 0.001), while the levels of MCP-1, IL-6 and CXCL1 derived from human mesangial cells when treated by IgAN-IgG-ddIgA1 and HC-IgG-ddIgA1 were comparable (MCP-1: 3701.1 ± 2199.9 pg/ml vs. 3373.9 ± 1465.6 pg/ml, p = 0.528; IL-6: 103.2 (81.5–277.4) pg/ml vs. 143.9 (108.2–248.6) pg/ml, p = 0.315; CXCL1: 1762.3 ± 934.0 pg/ml vs. 1575.8 ± 582.3 pg/ml; p = 0.383). In addition, monomeric ddIgA1 (mddIgA1) and polymeric ddIgA1 (pddIgA1), IgG derived from healthy controls (HC-IgG) and IgG derived from patients with IgAN (IgAN-IgG) were used as controls