狼疮中的免疫细胞信号缺陷：激活、失能与死亡。
Immune cell signaling defects in lupus: activation, anergy and death.
作者信息
Tsokos G C, Liossis S N
机构信息
Uniformed Services University of the Health Sciences, Dept of Medicine, Bethesda, MD 20814, USA.
出版信息
Immunol Today. 1999 Mar;20(3):119-24. doi: 10.1016/s0167-5699(98)01395-4.
Recent studies have identified novel aberrations in antigen receptor-mediated signaling events in lymphocytes from patients with systemic lupus erythematosus. Here, we propose that in lupus lymphocytes, the receptor-mediated increase in protein tyrosine phosphorylation and cytoplasmic free Ca2+ responses, along with T-cell receptor zeta chain deficiency, might explain the previously described diverse and conflicting immunoregulatory defects in human lupus.
最近的研究已经在系统性红斑狼疮患者的淋巴细胞中发现了抗原受体介导的信号转导事件中的新异常。在此，我们提出，在狼疮淋巴细胞中，受体介导的蛋白酪氨酸磷酸化增加和细胞质游离钙离子反应，以及T细胞受体ζ链缺陷，可能解释了先前描述的人类狼疮中多样且相互矛盾的免疫调节缺陷。
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