Laurence J, Gottlieb A B, Kunkel H G
J Clin Invest. 1983 Dec;72(6):2072-81. doi: 10.1172/JCI111172.
Supernatants from peripheral blood mononuclear cells obtained from certain patients with the acquired immune deficiency syndrome (AIDS) or its prodrome were capable of depressing spontaneous and pokeweed mitogen-driven B lymphocyte differentiation into plasmacytes, and the proliferative responses of T cells to specific antigen. These soluble suppressor factors (SSF) were present in uniquely high concentrations, with significant differences from healthy controls and from patients with various other conditions previously associated with factor-mediated immunosuppression. T cell-independent functions were not modified by SSF. Suppression was not genetically constrained, and did not appear to be mediated by cytotoxicity, prostaglandin, or alpha or gamma interferons. SSF was a product of the interaction of T lymphocytes with adherent cells. T cells or T cell factors from AIDS patients, but not from normal controls, could collaborate with control adherent cells in the formation of SSF. Restoration of DNA synthesis-independent differentiation of B lymphocytes into plasmacytes in SSF-treated cultures was realized by addition of reducing agents, such as 2-mercaptoethanol, on culture initiation. These data suggest inhibitory mechanisms possibly related to that of concanavalin A-induced soluble immune response suppression, and perhaps offer clues to clinically applicable substances which are potentially capable of mitigating such responses.
从某些获得性免疫缺陷综合征(AIDS)患者或其前驱症状患者获取的外周血单个核细胞的上清液,能够抑制自发的以及由商陆有丝分裂原驱动的B淋巴细胞分化为浆细胞,还能抑制T细胞对特异性抗原的增殖反应。这些可溶性抑制因子(SSF)以独特的高浓度存在,与健康对照以及先前与因子介导的免疫抑制相关的各种其他病症患者存在显著差异。不依赖T细胞的功能未被SSF改变。抑制作用不受遗传限制,并且似乎不是由细胞毒性、前列腺素或α或γ干扰素介导的。SSF是T淋巴细胞与贴壁细胞相互作用的产物。来自AIDS患者而非正常对照的T细胞或T细胞因子,可与对照贴壁细胞协同形成SSF。在培养开始时添加还原剂,如2-巯基乙醇,可使经SSF处理培养物中B淋巴细胞不依赖DNA合成而分化为浆细胞得以恢复。这些数据提示了可能与伴刀豆球蛋白A诱导的可溶性免疫反应抑制相关的抑制机制,或许还为潜在能够减轻此类反应的临床适用物质提供了线索。