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. Author manuscript; available in PMC: 2021 Feb 1.
Published in final edited form as: Kidney Int. 2019 Sep 5;97(2):340–349. doi: 10.1016/j.kint.2019.08.022

Figure 1. CpG-ODN stimulation induced production of nephritogenic IgA.

Figure 1.

Injection with CpG-ODN increased blood levels of aberrantly glycosylated IgA and IgG-IgA IC and exacerbated kidney injury in ddY mice. (A) ddY mice before development of IgAN were intra-peritoneally injected with CpG-ODN thrice weekly for 12 weeks. In histological analysis of glomerular lesions, CpG-ODN-injected mice showed mesangial cellular proliferation and extracellular matrix expansion. Right panel shows evaluation of renal injuries by semi-quantitative scoring. Renal histological scores, evaluated by percentages of glomeruli with aforementioned lesions, showed that renal injury in the mice injected with CpG-ODN were exacerbated. Urinary albumin levels in the CpG-ODN-injected mice were significantly elevated compared with those of control mice. Bars represent the mean±SEM. **P<0.01. (B) Immunohistochemical analysis of glomerular IgA, IgG, and C3 deposits. Only CpG-ODN-injected mice developed mesangial deposits of IgA, IgG, and C3. (C) Serum levels of IgA, IgG, and IgG-IgA IC were significantly increased after CpG-ODN treatment for 12 weeks. *P<0.05, **P<0.01. Serum IgA in mice injected with CpG-ODN showed significantly lower reactivity with lectin RCA-I and SNA lectins than the IgA in control mice. **P<0.01. These results indicate that injection of CpG-ODN increased serum levels of aberrantly glycosylated IgA. Individual points are shown. *P<0.05, **P<0.01.