Tsokos G C
Department of Clinical Physiology, Walter Reed Army Institute of Research, Washington, DC 20307-5100, USA.
Curr Opin Rheumatol. 1995 Sep;7(5):376-83. doi: 10.1097/00002281-199509000-00003.
Studies that were published over the past year have added new knowledge to our understanding of cellular abnormalities in systemic lupus erythematosus (SLE). Antigen-specific and "pathogenic" T cells can be identified and characterized in SLE. Interleukin-10 has been added to the factors that may promote B cell overactivity and autoantibody production. Protein kinase isozyme I was shown to be deficient in patients with SLE, indicating defects in cell signaling events. Aberrant expression of adhesion molecules on the surface membrane of leukocytes and endothelial cells was shown, with important mechanistic and therapeutic implications. Disruption of the lymphokine network (anti-interleukin-10 antibody) and the function of adhesion-costimulatory molecules (CTLA-4-immunoglobulin) were shown to be therapeutically significant in murine SLE.
过去一年发表的研究为我们对系统性红斑狼疮（SLE）细胞异常的理解增添了新知识。在SLE中可以识别并表征抗原特异性和“致病性”T细胞。白细胞介素-10已被纳入可能促进B细胞过度活跃和自身抗体产生的因素之中。已表明蛋白激酶同工酶I在SLE患者中缺乏，这表明细胞信号传导事件存在缺陷。已显示白细胞和内皮细胞表面膜上黏附分子的异常表达，具有重要的机制和治疗意义。在小鼠SLE中，淋巴因子网络的破坏（抗白细胞介素-10抗体）和黏附共刺激分子的功能（CTLA-4免疫球蛋白）在治疗上具有重要意义。
