Carpenter E A, Ruby J, Ramshaw I A
Division of Cell Biology, John Curtin School of Medical Research, Australian National University, Canberra, ACT.
J Immunol. 1994 Mar 15;152(6):2652-9.
The production of cytokines by virus immune spleen cells after in vitro restimulation was investigated. Vaccinia virus-primed spleen cells from CBA/H mice were stimulated in vitro with virus-infected UV-irradiated syngeneic cells. Both CD4+ and CD8+ T cell populations proliferated after restimulation. TNF, IL-6, and IFN-gamma were detected within 12 h of restimulation with maximal levels reached by 24 h. Adherent cells were major producers of IL-6 and TNF, whereas IFN-gamma production was dependent on CD4+ T cells and adherent cells. The IFN-gamma response was Ag specific, whereas the production of TNF and IL-6 was not. Stimulation with vaccinia virus constructs encoding IFN-gamma or TNF altered the levels of cytokines produced, in that IFN-gamma expression by stimulator cells led to increased IFN-gamma production, whereas TNF expression by stimulator cells augmented both TNF and IFN-gamma production by responder cells.
研究了体外再刺激后病毒免疫脾细胞产生细胞因子的情况。用病毒感染的紫外线照射的同基因细胞体外刺激来自CBA/H小鼠的经痘苗病毒致敏的脾细胞。再刺激后CD4+和CD8+ T细胞群体均增殖。再刺激后12小时内检测到TNF、IL-6和IFN-γ,24小时达到最高水平。贴壁细胞是IL-6和TNF的主要产生者,而IFN-γ的产生依赖于CD4+ T细胞和贴壁细胞。IFN-γ反应具有抗原特异性,而TNF和IL-6的产生则不具有。用编码IFN-γ或TNF的痘苗病毒构建体刺激改变了产生的细胞因子水平,即刺激细胞表达IFN-γ导致IFN-γ产生增加,而刺激细胞表达TNF则增强了应答细胞产生TNF和IFN-γ的能力。