Blasini A M, Stekman I L, Gonzalez F, Tositti M L, Rodriguez M A
Centro Nacional de Enfermedades Reumaticas, Hospital Universitario de Caracas, Venezuela.
Clin Immunol Immunopathol. 1994 Jan;70(1):66-72. doi: 10.1006/clin.1994.1012.
In the present study we have examined the potential contribution of IL-2/IL-2R interactions in CD3-mediated responses by T lymphocytes from patients with systemic lupus erythematosus (SLE). T-cells from SLE patients showed normal IL-2 production when activated with OKT3 MAb and submitogenic concentrations of PMA, in cultures in which uptake of endogenous IL-2 was prevented by pretreatment with anti-Tac MAb. In contrast, PHA-induced IL-2 production was lower in patients under the same conditions. Under these stimulatory conditions the proportions of T-cells expressing IL-2R CD25 molecules was comparable in patients and controls. There was earlier and higher binding of exogenously added IL-2 in T lymphocytes from patients activated via the CD3 pathway. Furthermore, these cells responded to IL-2 with stronger proliferative responses than cells from control subjects. These findings may partly explain the increased proliferative responses of SLE T-cells when stimulated via the CD3 pathway.
在本研究中,我们检测了白细胞介素-2(IL-2)/白细胞介素-2受体(IL-2R)相互作用在系统性红斑狼疮(SLE)患者T淋巴细胞的CD3介导反应中的潜在作用。当用OKT3单克隆抗体(MAb)和亚致有丝分裂浓度的佛波酯(PMA)激活时,在通过抗Tac MAb预处理防止内源性IL-2摄取的培养物中,SLE患者的T细胞显示出正常的IL-2产生。相比之下,在相同条件下,PHA诱导的患者IL-2产生较低。在这些刺激条件下,患者和对照中表达IL-2R CD25分子的T细胞比例相当。通过CD3途径激活的患者T淋巴细胞对外源性添加的IL-2有更早、更强的结合。此外,这些细胞对IL-2的增殖反应比对照受试者的细胞更强。这些发现可能部分解释了SLE T细胞在通过CD3途径刺激时增殖反应增加的原因。