Bhaskar Lakkakula Venkata Kameswara Subrahmanya, Nagaraju Ganji Purnachandra
Department of Zoology, Guru Ghasidas University, Bilaspur, 495009 (CG), India.
Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, GA 30322.
Crit Rev Immunol. 2019;39(5):343-360. doi: 10.1615/CritRevImmunol.2020033247.
Systemic lupus erythematosus (SLE) is an autoimmune disease triggered by a complex interaction of immunologic, environmental, and genetic factors. Like other diseases of autoimmune origin, SLE manifestations follow relapsing and remitting courses. Several lines of evidence have demonstrated the association of adaptive and innate immune responses with regulation in SLE pathogenesis. The immunological diagnosis primarily relies on detection of serum autoantibodies in SLE patients. A concordance rate of < 25% between monozygotic twins indicates potential involvement of environmental factors in SLE development. In addition, SLE is categorized by a wide range of clinical manifestations, partly related to the disease itself but also associated with comorbidities and adverse drug reactions. Because the common therapeutic strategies are connected with certain adverse events, immunosuppressive medications and biological agents are used on the basis of prevailing disease manifestations. Genome-wide association studies have identified 50 loci that influence SLE. However, the actual genetic polymorphism that imparts SLE risk is not fully known. Further understanding can help to expand quality of life in SLE individuals.
系统性红斑狼疮（SLE）是一种由免疫、环境和遗传因素复杂相互作用引发的自身免疫性疾病。与其他自身免疫性起源的疾病一样，SLE的表现呈复发和缓解病程。多条证据表明适应性免疫和先天性免疫反应与SLE发病机制中的调节相关。免疫诊断主要依赖于检测SLE患者血清中的自身抗体。同卵双胞胎之间<25%的一致率表明环境因素可能参与SLE的发病。此外，SLE具有广泛的临床表现，部分与疾病本身有关，但也与合并症和药物不良反应相关。由于常见的治疗策略会伴有某些不良事件，免疫抑制药物和生物制剂是根据主要的疾病表现来使用的。全基因组关联研究已经确定了50个影响SLE的基因座。然而，赋予SLE风险的实际基因多态性尚不完全清楚。进一步了解有助于提高SLE患者的生活质量。
