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系统性红斑狼疮(SLE)是一种以机体产生大量病理性抗核蛋白和抗DNA自身抗体为特征的自身免疫疾病。近年的研究发现,患者体内异常升高的IFN-α是触发SLE病理性免疫应答,进而导致病理损伤的中心环节。实验发现来源于SLE患者的免疫复合物(SLE-ICs)可激活外周血单核细胞(PBMC),而来源于其他非SLE自身免疫病患者的ICs(non-SLE-ICs)不具有这种活性。进一步观察发现,SLE-ICs能够刺激PBMC中的浆细胞样树突状细胞(pDCs),单核细胞,B细胞和预先用巨噬细胞-粒细胞集落刺激因子(GM-CSF)处理过的多型核白细胞(PMN)活化并分泌IL-8,而对T细胞,
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the body’s production of a large number of pathological anti-nuclear proteins and anti-DNA autoantibodies. In recent years, the study found that patients with abnormally elevated IFN-α is to trigger SLE pathological immune response, which led to the central part of pathological injury. It has been found that immune complexes (SLE-ICs) from SLE patients activate peripheral blood mononuclear cells (PBMCs), whereas ICs (non-SLE-ICs) from other non-SLE autoimmune diseases do not possess this activity . Further observation showed that SLE-ICs stimulated the proliferation of plasmacytoid dendritic cells (PBMCs), monocytes, B cells and pre-treated with macrophage-granulocyte colony-stimulating factor (GM-CSF) Type of nucleolar leukocytes (PMN) activation and secretion of IL-8, and T cells,