系统性红斑狼疮中的免疫细胞生化异常。

Immune cell biochemical abnormalities in systemic lupus erythematosus.

作者信息

Liossis S N, Vassilopoulos D, Kovacs B, Tsokos G C

机构信息

Department of Clinical Physiology, Walter Reed Army Institute of Research, Washington, DC 20307-5100, USA.

出版信息

Clin Exp Rheumatol. 1997 Nov-Dec;15(6):677-84.

PMID:9444427

Abstract

Novel data have emerged which attempt to characterize the biochemical abnormalities that are exhibited by lupus immune cells. Lupus lymphocytes display abnormal antigen-receptor-mediated signaling, consisting of increased Ca2+ mobilization and increased protein tyrosyl phosphorylation that are independent of disease activity. Abnormalities in the expression and function of co-stimulatory molecules (B7-CD28 and CD40-CD40L) have been established. Transcription of cytokine genes and the methylation of DNA which affects multiple genes are also abnormal. Finally, aberrations of the apoptosis of lupus immune cells are contributors to the pathogenesis of the disease.

摘要

新的数据已经出现，这些数据试图描述狼疮免疫细胞所表现出的生化异常。狼疮淋巴细胞表现出异常的抗原受体介导信号传导，包括增加的钙离子动员和增加的蛋白酪氨酸磷酸化，且这些都与疾病活动无关。共刺激分子（B7-CD28和CD40-CD40L）的表达和功能异常已得到证实。细胞因子基因的转录以及影响多个基因的DNA甲基化也不正常。最后，狼疮免疫细胞凋亡异常是该疾病发病机制的促成因素。