狼疮性肾炎
免疫学
脾细胞
抗体
分子生物学
肿瘤坏死因子α
系统性红斑狼疮
红斑狼疮
化学
生物
医学
内科学
疾病
作者
Hong Li,Yunyi Zhang,Yanan Sun,Xiyi Huang,Yongfeng Jia,Li Duan
摘要
AIM:
To establish an animal model for systemic lupus erythematosus (SLE)-like syndrome in mice.
METHODS:
BALB/c mice were immunized with active chromatin isolated from ConA-activated syngeneic spleno-lymphocytes. Plasma samples of mice were tested by enzyme-linked immunosorbent assays (ELISA) for the presence of IgG anti-dsDNA, -ssDNA, and anti-histone antibodies. Tumor necrosis factor-alpha (TNF-alpha) in serum was measured by ELISA. Spleno-lymphocyte proliferation assays and the levels of interferon-gamma (IFN-gamma) in supernatants were tested respectively. Proteinuria was measured. Kidneys were examined by direct immunohistochemical method and light microscopy.
RESULTS:
Anti-ds DNA, ssDNA, and histone antibodies were induced in active chromatin-immunized mice, the proliferation response of splenocytes to ConA and LPS were reduced, levels of interferon-gamma in supernatants and TNF-alpha in serum were lowered. Lupus nephritis was assessed by the presence of Ig deposits, glomerular pathology and proteinuria.
CONCLUSION:
The active chromatin-induced SLE-like mouse model was similar to idiopathic SLE in human.
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