Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
Arthritis Res Ther. 2011 Mar 17;13(2):207. doi: 10.1186/ar3251.
Systemic lupus erythematosus (SLE) is an autoimmune disease resulting from a loss of tolerance to multiple self antigens, and characterized by autoantibody production and inflammatory cell infiltration in target organs, such as the kidneys and brain. T cells are critical players in SLE pathophysiology as they regulate B cell responses and also infiltrate target tissues, leading to tissue damage. Abnormal signaling events link to defective gene transcription and altered cytokine production, contributing to the aberrant phenotype of T cells in SLE. Study of signaling and gene transcription abnormalities in SLE T cells has led to the identification of novel targets for therapy.
系统性红斑狼疮(SLE)是一种自身免疫性疾病,由对多种自身抗原的耐受性丧失引起,其特征是在肾脏和大脑等靶器官中产生自身抗体和炎症细胞浸润。T 细胞是 SLE 病理生理学中的关键参与者,因为它们调节 B 细胞反应,也浸润靶组织,导致组织损伤。异常信号事件与缺陷基因转录和细胞因子产生改变相关,导致 SLE T 细胞的异常表型。对 SLE T 细胞中信号转导和基因转录异常的研究导致了治疗的新靶点的确定。