Comprehensive Arthritis, Musculoskeletal, and Autoimmunity Center, Department of Medicine, University of Alabama at Birmingham, USA.
Autoimmun Rev. 2010 May;9(7):473-6. doi: 10.1016/j.autrev.2010.02.003. Epub 2010 Feb 8.
Systemic lupus erythematosus (SLE) is a complex autoimmune disorder marked by an inappropriate immune response to nuclear antigens. Recent whole genome association and more focused studies have revealed numerous genes implicated in this disease process, including ITGAM, Fc gamma receptors, complement components, C-reactive protein, and others. One common feature of these molecules is their involvement in the immune opsonin pathway and in phagocytic clearing of nuclear antigens and apoptotic debris, which provide excessive exposure of lupus-related antigens to immune cells. Analysis of gene-gene interactions in the opsonin pathway and its relationship to SLE may provide a system-based approach to identify additional candidate genes associated with disease able to account for a larger part of lupus susceptibility.
系统性红斑狼疮（SLE）是一种复杂的自身免疫性疾病，其特征是对核抗原产生不适当的免疫反应。最近的全基因组关联和更集中的研究揭示了许多参与这一疾病过程的基因，包括 ITGAM、Fc 受体、补体成分、C 反应蛋白等。这些分子的一个共同特征是它们参与免疫调理途径和核抗原及凋亡碎片的吞噬清除，这为免疫细胞提供了过多的狼疮相关抗原暴露。对调理素途径中的基因-基因相互作用及其与 SLE 的关系进行分析，可能为识别与疾病相关的其他候选基因提供一种基于系统的方法，这些基因能够解释狼疮易感性的更大部分。
