Tsokos G C
Department of Clinical Physiology, Walter Reed Army Institute of Research, Washington, DC 20307-5100, USA.
Curr Opin Rheumatol. 1996 Sep;8(5):395-402. doi: 10.1097/00002281-199609000-00002.
Studies reported during the past year have added new knowledge to our understanding of cellular abnormalities in systemic lupus erythematosus: 1) Antigen-specific and "pathogenic" T cells display a limited T cell receptor repertoire in lupus. 2) The ratio of interleukin-10 to interferon gamma-secreting cells in the peripheral blood of patients with lupus is increased in patients with active disease. 3) CD3-mediated increases in free intracytoplasmic calcium occur specifically in lupus T cells and lines; this finding provides additional evidence that cell-signaling events are defective in patients with lupus. 4) Aberrant expression of adhesion molecules on the surface membrane of leukocytes and endothelial cells was shown, a finding with important mechanistic and therapeutic implications. 5) Lupus antigen-presenting cells fail to upregulate the expression of B7-1 (CD80) in response to interferon gamma; defective expression of B7-1 is responsible for the decreased response of lupus cells to recall antigens.
1）抗原特异性和“致病性”T细胞在狼疮中表现出有限的T细胞受体库。2）狼疮患者活动期外周血中白细胞介素-10与分泌干扰素γ的细胞的比例增加。3）CD3介导的游离胞浆内钙增加特别发生在狼疮T细胞和细胞系中；这一发现为狼疮患者细胞信号事件存在缺陷提供了额外证据。4）白细胞和内皮细胞表面膜上粘附分子的异常表达被证实，这一发现具有重要的机制和治疗意义。5）狼疮抗原呈递细胞在干扰素γ刺激下未能上调B7-1（CD80）的表达；B7-1的表达缺陷导致狼疮细胞对回忆抗原的反应降低。
