Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02115, USA.
Nat Rev Rheumatol. 2010 Jun;6(6):317-25. doi: 10.1038/nrrheum.2010.60. Epub 2010 May 11.
T cells contribute to the initiation and perpetuation of autoimmunity in systemic lupus erythematosus (SLE), and seem to be directly involved in the development of related organ pathology. Defects associated with CD8(+) and T-regulatory (T(REG)) cell function manifest in parallel with the expanded CD3(+)CD4(-)CD8(-) T cell lineage. The cytokine expression pattern is uniquely characterized by decreased expression of interleukin (IL)-2 and increased production of IL-17 and related cytokines. Therapeutic approaches that limit the cognate interaction between T cells and B cells, prevent inappropriate tissue homing and restore T(REG) cell function and the normal cytokine milieu have been entertained. Biochemical characterization of SLE T cells has revealed distinct early and late signaling aberrations, and has enabled the identification of novel molecular targets that can be corrected with small molecules, and biomarkers that may foretell disease activity and predict organ damage.
T 细胞有助于全身性红斑狼疮（SLE）的自身免疫的起始和持续，并似乎直接参与相关器官病理学的发展。与 CD8(+)和 T 调节（T(REG)）细胞功能相关的缺陷与扩展的 CD3(+)CD4(-)CD8(-)T 细胞谱系同时出现。细胞因子表达模式的特征是白细胞介素（IL）-2 的表达降低，IL-17 和相关细胞因子的产生增加。已经尝试了限制 T 细胞和 B 细胞之间的同源相互作用、防止不当组织归巢以及恢复 T(REG)细胞功能和正常细胞因子环境的治疗方法。SLE T 细胞的生化特征揭示了明显的早期和晚期信号异常，并使能够鉴定可以用小分子纠正的新型分子靶标，以及可能预示疾病活动和预测器官损伤的生物标志物。
