Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA.
J Interferon Cytokine Res. 2011 Oct;31(10):769-79. doi: 10.1089/jir.2011.0029. Epub 2011 Aug 30.
Systemic lupus erythematosus (SLE) is an autoimmune disease associated with chronic immune activation and tissue damage. Organ damage in SLE results from the deposition of immune complexes and the infiltration of activated T cells into susceptible organs. Cytokines are intimately involved in every step of the SLE pathogenesis. Defective immune regulation and uncontrolled lymphocyte activation, as well as increased antigen presenting cell maturation are all influenced by cytokines. Moreover, expansion of local immune responses as well as tissue infiltration by pathogenic cells is instigated by cytokines. In this review, we describe the main cytokine abnormalities reported in SLE and discuss the mechanisms that drive their aberrant production as well as the pathogenic pathways that their presence promotes.
系统性红斑狼疮（SLE）是一种自身免疫性疾病，与慢性免疫激活和组织损伤有关。SLE 中的器官损伤是由免疫复合物的沉积和活化的 T 细胞浸润到易感器官引起的。细胞因子在 SLE 发病机制的每一个步骤中都密切参与。细胞因子影响缺陷的免疫调节和失控的淋巴细胞激活，以及抗原提呈细胞的成熟。此外，细胞因子还引发局部免疫反应的扩张以及致病细胞对组织的浸润。在这篇综述中，我们描述了在 SLE 中报道的主要细胞因子异常，并讨论了驱动它们异常产生的机制以及它们存在促进的致病途径。
