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细胞凋亡缺陷是系统性红斑狼疮发病机制之一。细胞凋亡机制的失衡导致自身抗体的产生。这些抗体缺乏区分致病性和正常宿主细胞的能力,导致细胞死亡增加和免疫耐受异常(Andrade et al. 2000;Rahman和Isenberg 2008)。据认为,免疫系统的所有主要成分在不同程度上参与SLE的进展。大多数存在于细胞核中的蛋白质都是免疫系统的靶点。SLE可能的环境诱因包括紫外线、药物和病毒。这些刺激会破坏细胞,暴露细胞的DNA、组蛋白和其他蛋白质,尤其是细胞核的一部分。可见SLE患者单核细胞和角质形成细胞死亡增加,免疫系统B细胞和T细胞Fas蛋白超表达。刺痛性体巨噬细胞(TBMs)是存在于次生淋巴结生发中心的大型吞噬细胞。它们表达CD68蛋白。这些细胞通常吞噬体细胞超突变后凋亡的B细胞。在一些SLE患者中,TBMs明显减少,且这些细胞很少含有凋亡B细胞的物质。此外,TBMs外也可发现未摄取的凋亡细胞核。该物质可能对B细胞和T细胞的甲酰化产生威胁.


Defects in apoptosis are one of the proposed mechanisms involved in patho-physiological events of SLE. Imbalance in apoptotic machinery leads to the production of auto-antibodies. These antibodies lack the ability to differentiate between pathogenic and normal host cells and cause increase cell death and abnormalities in immune tolerance (Andrade et al. 2000; Rahman and Isenberg 2008). It is believed that all the major components of immune system are involved in SLE progression at various levels. Mostly proteins present in cell nucleus are targeted by the immune system. The likely environmental triggers for SLE include ultraviolet light, drugs, and viruses. These stimuli cause the destruction of cells and expose their DNA, histones, and other proteins, particularly parts of the cell nucleus. It is observed that in patients suffering from SLE, there is increased cell death in monocytes and keratinocytes and hyper expression of Fas protein by B and T cells of the immune system. Tingible body macrophages (TBMs) are large phagocytic cells present in the germinal centers of secondary lymph nodes. They express CD68 protein. These cells normally engulf B cells which have undergone apoptosis after somatic hypermutation. In some patients with SLE, significantly fewer TBMs can be found, and these cells rarely contain material from apoptotic B cells. Also, uningested apoptotic nuclei can be found outside of TBMs. This material may present a threat to the tolerization of B cells and T cells


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