Punnonen J
Department of Medical Microbiology, University of Turku, Finland.
Clin Exp Immunol. 1989 Mar;75(3):421-6.
The effect of interleukin 2 (IL-2) on cord blood mononuclear cells (CBMC) was studied, with special reference to B cell function. The study shows that CBMCs proliferate in response to recombinant interleukin 2 (rIL-2) without in-vitro preactivation. The response was also detected when whole blood cultures were used. CBMCs not preactivated in vitro proliferated in response to rIL-2 even after T cell and monocyte depletion. Thus, rIL-2 affects both non-T cells and T cells of newborns without preactivation in vitro. IL-2 receptors on unstimulated CBMCs appear to be distinct from Tac antigen, as the mean number of Tac antigen-positive cells among CBMCs was only 0.8%. Furthermore, rIL-2 inhibited PWM-induced proliferation and the response was more prominent in newborns than in adults. Thus, rIL-2 seems to cause a higher increase of suppressor cell function in CBMCs than in adult peripheral blood mononuclear cells. Neither rIL-2 nor Staphylococcus aureus Cowan 1 (SAC) stimulated any IgM synthesis, but a dose-dependent IgM synthesis was obtained by combining SAC and rIL-2. Alone, however, rIL-2 appears to be an insufficient factor to induce differentiation of SAC-activated cord blood B cells, as no IgM production in response to rIL-2 occurred in T cell and monocyte-depleted cell populations. The results of this study suggest both increased suppressor cell function and intrinsic B cell deficiency as causes of a weak humoral immune response in newborns.
研究了白细胞介素2(IL-2)对脐血单个核细胞(CBMC)的作用,特别关注B细胞功能。研究表明,CBMC在无体外预激活的情况下对重组白细胞介素2(rIL-2)产生增殖反应。使用全血培养时也检测到了这种反应。即使在T细胞和单核细胞去除后,未在体外预激活的CBMC对rIL-2仍有增殖反应。因此,rIL-2在无体外预激活的情况下影响新生儿的非T细胞和T细胞。未刺激的CBMC上的IL-2受体似乎与Tac抗原不同,因为CBMC中Tac抗原阳性细胞的平均数量仅为0.8%。此外,rIL-2抑制PWM诱导的增殖,且这种反应在新生儿中比在成年人中更明显。因此,rIL-2似乎比在成人外周血单个核细胞中更能引起CBMC中抑制细胞功能的更高增强。rIL-2和金黄色葡萄球菌Cowan 1(SAC)均未刺激任何IgM合成,但通过将SAC和rIL-2联合使用可获得剂量依赖性的IgM合成。然而,单独的rIL-2似乎是诱导SAC激活的脐血B细胞分化的不足因素,因为在T细胞和单核细胞去除的细胞群体中未出现对rIL-2的IgM产生。本研究结果表明,抑制细胞功能增强和内在B细胞缺陷均是新生儿体液免疫反应较弱的原因。