Crispín José C, Kyttaris Vasileios, Juang Yuang-Taung, Tsokos George C
Division of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, 4 Blackfan Circle, HIM-244, Boston, MA 02115, USA.
Ann Rheum Dis. 2007 Nov;66 Suppl 3(Suppl 3):iii65-9. doi: 10.1136/ard.2007.078493.
T cells from patients with systemic lupus erythematosus exhibit a notable array of defects that probably contribute to the origin and development of the disease. Such abnormalities include an abnormal response to stimulation, aberrant expression of molecules that play key roles in intracellular signalling pathways, altered transcription factor activation and binding, and skewed gene expression. The combination of these alterations leads the cell to the expression of a particular phenotype that intense research has gradually uncovered over the last years. The aim of this article is to review the findings that have allowed us to better understand the behaviour of the lupus T cell and highlight the molecules that represent potential therapeutic targets.
系统性红斑狼疮患者的T细胞表现出一系列显著缺陷,这些缺陷可能促成了该疾病的起源和发展。此类异常包括对刺激的异常反应、在细胞内信号通路中起关键作用的分子的异常表达、转录因子激活和结合的改变以及基因表达的偏差。这些改变的综合作用导致细胞呈现出一种特定表型,在过去几年中,深入研究已逐渐揭示了这种表型。本文旨在综述相关研究结果,这些结果使我们能够更好地理解狼疮T细胞的行为,并着重介绍那些代表潜在治疗靶点的分子。