白细胞介素-6在ALD-DNA诱导的SLE模型小鼠SLE中的作用机制研究

目的探讨白细胞介素(IL)-6对ALD-DNA诱导的系统性红斑狼疮(SLE)模型小鼠SLE中的作用机制。方法在健康的雌性C57BL/6小鼠体内用活化淋巴细胞来源的DNA(ALD-DNA)免疫,从而诱导小鼠的SLE,未免疫的小鼠被用作对照。检测了疾病相关的一些发病指标,包括抗双链DNA抗体,尿蛋白和肾脏的病理学改变。结果 IL-6KO基因敲除的小鼠能抵抗ALD-DNA诱导的小鼠SLE模型。在IL-6KO免疫的小鼠中,CD4~+T细胞的活化状态低于野生型的免疫小鼠。胞内细胞因子染色结果表明,IL-6KO免疫的小鼠体内Foxp3的表达高于野生型免疫的小鼠。结论在ALD-DNA诱导的SLE模型中,IL-6可以抑制Treg细胞的分化,从而促进疾病的发展。

The mechanism of interleukin-6 on SLE in systemic lupus erythematosus mouse model induced by ALD-DNA

Objective To investigate the mechanism of interleukin(IL )-6 on the systemic lupus erythematosus mouse model of systemic lupus erythematosus in ALD-DNA induced .Methods The source of activated lymphocytes in mice with normal female C57BL/6 DNA(ALD-DNA)immunity ,systemic lupus erythematosus and induced mice ,non immune mice were used as controls .De-tection of some indexes related to the disease onset ,including anti double stranded DNA antibody ,changes of urinary protein and kidney pathology .Results IL-6 knockout mice were able to resist the model of ALD-DNA induced systemic lupus erythematosus . In IL-6 KO immunized mice ,the activation state of CD4 + T cells was lower than that of wild type mice .Intracellular cytokine stai-ning indicated that the expression of IL-6 KO immune mice Foxp3 was higher than that of wild type mice immunized .Conclusion The systemic lupus erythematosus model induced by ALD-DNA in differentiation of IL-6 could inhibit Treg ,so as to promote the development of the disease .