Mirza N M, Relias V, Yunis E J, Pachas W N, Dasgupta J D
Division of Immunogenetics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.
Hum Immunol. 1993 Feb;36(2):91-8. doi: 10.1016/0198-8859(93)90111-d.
T cells from patients with active RA are known to produce low levels of IL-2 and proliferate poorly in response to various mitogenic stimuli. The present work shows that cross-linking of CD3 antigen on patients' T-cell surface induces two- to threefold lower Ca2+ response than in T cells from age-matched controls. Immunofluorescence studies indicate that the attenuated signal may be due to the suppressed expression of CD3 and/or CD45 molecules on patients' T cells. In the majority of the patients, the level of CD45 expression is reduced by 60%-70% as compared with that in the control T cells. Therefore, the poor mitogenic response of patient cells is apparently due to a defect in early stages of signal transduction through the T-cell receptor (TCR-CD3).
已知活动性类风湿关节炎（RA）患者的T细胞产生低水平的白细胞介素-2（IL-2），并且对各种促有丝分裂刺激的增殖能力较差。目前的研究表明，患者T细胞表面CD3抗原的交联诱导的Ca2+反应比年龄匹配对照组的T细胞低两到三倍。免疫荧光研究表明，信号减弱可能是由于患者T细胞上CD3和/或CD45分子的表达受到抑制。在大多数患者中，与对照T细胞相比，CD45的表达水平降低了60%-70%。因此，患者细胞促有丝分裂反应不佳显然是由于通过T细胞受体（TCR-CD3）的信号转导早期存在缺陷。
