Blasini A M, Alonzo E, Chacón R, Riera R, Stekman I L, Rodriguez M A
Centro Nacional de Enfermedades Reumáticas, Hospital Universitario de Caracas, Venezuela.
Lupus. 1998;7(8):515-23. doi: 10.1191/096120398678920604.
Previous reports have shown abnormal responses mediated via the TCR/CD3 pathway in T lymphocytes from systemic lupus erythematosus (SLE) patients. Recently, we and others have reported augmented TCR/CD3-mediated responses in lupus T cells. It is possible that the pattern of downstream biochemical signals triggered by TCR/CD3 ligation may be altered in T lymphocytes from patients with SLE, thus leading to abnormal distal cell responses. In this paper we have examined the phosphorylation of proteins on tyrosine residues in peripheral blood T lymphocytes from a group of SLE patients and controls. We found a lower frequency of constitutively tyrosine-phosphorylated 119- and 113-kDa substrates and an enhanced frequency of tyrosine-phosphorylated 66- and 25-kDa proteins in unstimulated cultures of SLE T lymphocytes, suggesting an altered pattern of tyrosine phosphorylation in T cells from patients in vivo. Additionally, the protein tyrosine phosphatase (PTP) activity of CD45 immunoprecipitates was lower in unstimulated lupus T cells and was enhanced after stimulation via the CD3 pathway in lupus but not control T lymphocytes. The present results seem to suggest abnormal regulation of in-vivo tyrosine phosphorylation in T cells from patients with SLE.
先前的报告显示，系统性红斑狼疮（SLE）患者的T淋巴细胞中通过TCR/CD3途径介导的反应异常。最近，我们和其他人报告了狼疮T细胞中TCR/CD3介导的反应增强。SLE患者的T淋巴细胞中，由TCR/CD3连接触发的下游生化信号模式可能发生改变，从而导致远端细胞反应异常。在本文中，我们检测了一组SLE患者和对照者外周血T淋巴细胞中酪氨酸残基上蛋白质的磷酸化情况。我们发现，在未刺激的SLE T淋巴细胞培养物中，组成型酪氨酸磷酸化的119 kDa和113 kDa底物的频率较低，而酪氨酸磷酸化的66 kDa和25 kDa蛋白质的频率增加，这表明体内患者T细胞中酪氨酸磷酸化模式发生了改变。此外，在未刺激的狼疮T细胞中，CD45免疫沉淀物的蛋白酪氨酸磷酸酶（PTP）活性较低，并且在狼疮T淋巴细胞中通过CD3途径刺激后增强，但在对照T淋巴细胞中未增强。目前的结果似乎表明SLE患者T细胞中体内酪氨酸磷酸化存在异常调节。
