Pryjma J, Mytar B, Loppnow H, Ernst M, Zembala M, Flad H D
Department of Clinical Immunology and Microbiology, Copernicus Medical School, Cracow, Poland.
Immunology. 1992 Feb;75(2):355-60.
Monocyte subpopulations which differ in the expression of Fc receptor for human IgG (FcRI) differentially regulate the T-cell-dependent, pokeweed mitogen (PWM)-induced, polyclonal B-cell response. We, thus, studied the cytokine production in human peripheral blood monocyte and T-lymphocyte cultures activated with this lectin. Monocytes or their FcR+ and FcR- subpopulations stimulated with PWM were cultured with or without T lymphocytes or their CD4+ and CD8+ subsets. Both monocyte subpopulations cultured alone produced similar amounts of tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), but FcR- monocytes showed significantly enhanced ability to secrete interleukin-1 (IL-1). T cells, especially CD4+, added to monocyte cultures enhanced IL-1 production. This enhancement was presumably due to interferon-gamma (IFN-gamma) release by T lymphocytes, since this lymphokine enhanced IL-1 secretion when added to PWM-stimulated cultures of monocytes. Addition of monocytes, in particular the FcR+ subpopulation, greatly enhanced production of IFN-gamma by T lymphocytes. Although both T-cell subsets produced IFN-gamma, the CD4+ cells were more efficient. These results indicate that in PWM-stimulated cultures subpopulations of monocytes differ in secretion of cytokines, which might explain their differential effect on T-cell-dependent immune responses in vitro.
表达人IgG Fc受体(FcRI)不同的单核细胞亚群对T细胞依赖性、商陆丝裂原(PWM)诱导的多克隆B细胞反应具有不同的调节作用。因此,我们研究了用这种凝集素激活的人外周血单核细胞和T淋巴细胞培养物中的细胞因子产生情况。用PWM刺激的单核细胞或其FcR +和FcR-亚群与T淋巴细胞或其CD4 +和CD8 +亚群一起或不一起培养。单独培养的两个单核细胞亚群产生相似量的肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6),但FcR-单核细胞显示出显著增强的分泌白细胞介素-1(IL-1)的能力。添加到单核细胞培养物中的T细胞,尤其是CD4 +细胞,增强了IL-1的产生。这种增强可能是由于T淋巴细胞释放干扰素-γ(IFN-γ),因为当添加到PWM刺激的单核细胞培养物中时,这种淋巴因子增强了IL-1的分泌。添加单核细胞,特别是FcR +亚群,极大地增强了T淋巴细胞产生IFN-γ的能力。虽然两个T细胞亚群都产生IFN-γ,但CD4 +细胞更有效。这些结果表明,在PWM刺激的培养物中,单核细胞亚群在细胞因子分泌方面存在差异,这可能解释了它们在体外对T细胞依赖性免疫反应的不同影响。