The significance of bcl-2 in production of galactose-deficient IgA1 in IgA nephropathy

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462678
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Otorhinolaryngology
• Research Institution: University of Fukui
• Principal Investigator: SUNAGA HIROSI 福井大学, 医学部, 特別研究員 (30362049)
• Co-Investigator(Kenkyū-buntansha): FUJIEDA SHIGEHARU 福井大学, 医学部, 教授 (30238539)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: IgA腎症 / 口蓋扁桃 / 病巣感染症

Outline of Final Research Achievements

In this study, we demonstrated that the level of bcl-2 was significantly increased in tonsil mononuclear cells from the patients with IgA nephropathy compare to control sample. In peripheral mononuclear cells, the level of bcl-2 was also increased, significantly. Since galactose-deficient IgA1 is involved in pathogenesis of IgA nephropathy, our results suggest that bcl-1 might play pivotal role in production of galactose-deficient IgA1. We therefore study the influences of bcl-2 on production of galactose-deficient IgA1. Stimulation of lipopolysaccharide (LPS) or H. Parainfluenzae (HP antigen) on peripheral mononuclear cells induce up-regulation of galactose-deficient IgA1 in supernatant by using ELISA. However, suppression of bcl-2 did not influence the production of galactose-deficient IgA1. Therefore, we could not any correlation between bcl-2 and galactose-deficient IgA1. Further study is required to elucidate the mechanism by which bcl-2 induce IgA nephropathy.

Free Research Field

IgA腎症