Mesangial viral and psuedoviral immunity: possible involvement in the pathogenesis of glomerulonephritis

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461615
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pediatrics
• Research Institution: Hirosaki University
• Principal Investigator: Tanaka Hiroshi 弘前大学, 教育学部, 教授 (50271820)
• Co-Investigator(Kenkyū-buntansha): IMAIZUMI TADAATSU 弘前大学, 大学院医学研究科, 教授 (90232602) ; YOSHIDA HIDEMI 弘前大学, 大学院医学研究科, 講師 (40201008)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 腎炎症候群 / 自然免疫 / メサンギウム細胞 / 炎症性ケモカイン / メサンギウム細胞

Outline of Final Research Achievements

Since viral infections activate type I interferon (IFN) pathways and cause subsequent release of IFN-dependent proinflammatory chemokines/cytokines, the innate immune system plays an important role in the pathogenesis of
glomerulonephritis (GN). So far, we have examined the toll-like receptor (TLR) 3 signaling cascades treated with polyinosinic-polycytidylic acid (poly IC), a synthetic analogue of viral dsRNA, that makes “pseudoviral” infection in cultured human mesangial cells (MCs). We found that the activation of mesangial TLR3 upregulated the expression of functional molecules acting as monocyte/macrophage and lymphocyte chemoattractants in MCs. Further, intense glomerular expressions of these functional molecules were observed in biopsy specimens from children with　GN. These observations further support the implication of “pseudoviral” immunity in the pathogenesis of GN.

Free Research Field

小児腎臓病学