Crispín José C, Tsokos George C
Division of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, 4 Blackfan Circle, HIM-244, Boston, MA 02115, USA.
Autoimmun Rev. 2008 Jan;7(3):256-61. doi: 10.1016/j.autrev.2007.11.020. Epub 2007 Dec 4.
T cells from patients with systemic lupus erythematosus (SLE) display a number of biochemical abnormalities which include altered expression of key signaling molecules, heightened calcium responses, and skewed expression of transcription factors. These defects are involved in the altered behavior of SLE T cells and are probably central in the disease pathogenesis. The aim of this communication is to review the defects that have been consistently documented in SLE T cells, highlighting molecules and pathways that represent therapeutic targets.
系统性红斑狼疮(SLE)患者的T细胞表现出许多生化异常,包括关键信号分子表达改变、钙反应增强以及转录因子表达失衡。这些缺陷与SLE T细胞行为改变有关,可能在疾病发病机制中起核心作用。本通讯旨在综述SLE T细胞中一直有记录的缺陷,重点介绍代表治疗靶点的分子和途径。