Liu T F, Jones B M
Department of Pathology, University of Hong Kong, Hong Kong.
Cytokine. 1998 Feb;10(2):140-7. doi: 10.1006/cyto.1997.0268.
Interleukin 12 (IL-12) plays a crucial role in defensive immune responses, modulation of cytokine production and is involved in the pathogenesis of some autoimmune diseases. The authors investigated whether decreased in vitro production of IL-12 occurs in systemic lupus erythematosus (SLE), in which the cytokine secreting pattern is predominantly type 2. IL-12 production by SLE peripheral blood mononuclear cells (PBMC) was significantly impaired compared with normal PBMC, and this was not due to decreased numbers of monocytes. After depletion of non-adherent cells from PBMC, monocytes of SLE patients produced significantly less IL-12 than those of controls, but IL-12 levels in SLE and control non-adherent cells supernatants were not significantly different. Exogenous recombinant (r)IL-10 strongly inhibited IL-12 production by both SLE and normal PBMC and anti-IL-10 neutralizing antibody significantly reversed the IL-12 deficiency of SLE PBMC and SLE monocytes, while not affecting normal PBMC. Recombinant interferon gamma (rIFN-gamma) considerably enhanced IL-12 production in both SLE and normal PBMC, but it did not significantly reverse the inhibitory effect of rIL-10 on IL-12 production. IL-12 production was significantly lower in patients with active SLE than those in remission. These results suggest that SLE monocytes may be deficient in IL-12 production and that this is secondary to abnormal production of various cytokines, especially excessive production of IL-10.
白细胞介素12(IL-12)在防御性免疫反应、细胞因子产生的调节中起关键作用,并参与某些自身免疫性疾病的发病机制。作者研究了系统性红斑狼疮(SLE)中是否存在体外IL-12产生减少的情况,在SLE中细胞因子分泌模式主要为2型。与正常外周血单个核细胞(PBMC)相比,SLE患者PBMC产生IL-12的能力明显受损,这并非由于单核细胞数量减少所致。从PBMC中去除非贴壁细胞后,SLE患者的单核细胞产生的IL-12明显少于对照组,但SLE和对照非贴壁细胞上清液中的IL-12水平无显著差异。外源性重组(r)IL-10强烈抑制SLE和正常PBMC产生IL-12,抗IL-10中和抗体显著逆转SLE PBMC和SLE单核细胞的IL-12缺乏,而不影响正常PBMC。重组干扰素γ(rIFN-γ)显著增强SLE和正常PBMC中IL-12的产生,但它并未显著逆转rIL-10对IL-12产生的抑制作用。活动期SLE患者的IL-12产生明显低于缓解期患者。这些结果表明,SLE单核细胞可能存在IL-12产生缺陷,这是各种细胞因子异常产生的继发结果,尤其是IL-10的过度产生。