The analysis of new mouse model for glomerulonephritis and an approach for Th1/Th2 cell regulation by transcription factors

点击翻译按钮获取中文摘要

Flsky skin (fsn) mice develop glomerulonephritis, psoriasis, a high level of serum IgE, and severe anemia. Psoriasis is known to Th1 phenotype and a high level of IgE is Th2 phenotype. The transcription factors T-bet and GATA-3 are thought to be key regulators of Th1/Th2 differentiation. In this study, T-bet overexpressed fsn mice (T-bet fsn mice) and GATA-3 overexpressed fsn mice (GATA-3 fsn mice) were generated and analyzed with fsn mice about glomerulonephritis and Th1/Th2 subset. The results showing as following : 1. fsn mice showed CD4/CD8 imbalance. Thymus CD4+CD8+ T cells population in fsn mice was decreased than that of wild mice. 2. The proteinuria of T-bet fsn mice decreased than that of fsn mice. The results suggested that transcriptional regulation might effect the development of glomerulonephritis in fsn mice. 3. fsn mice showed Th2 dominant background in immunoglobulin subset analysis. 4. T-bet fsn mice showed Th1 dominant background in immunoglobulin subset analysis. The serum IgG1 level and IgG2a/IgG1 ratio of T-bet fsn mice was lower than those of fsn mice. 5. T-bet fsn mice did not prolong the survival rate than that of fsn mice. T-bet fsn mice, GATA-3 fsn mice, and fsn mice all died within 25 week-old. The results showed that T-bet overexpressed in fsn mice might improve glomerulonephritis, but not survival rate. The data suggested that Th1/Th2 background might not contribute the cause of death in fsn mice. The cause of death in fsn mice might be due to other reasons, such as severe anemia.