Badovinac V P, Corbin G A, Harty J T
Department of Microbiology and Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, IA 52242, USA.
J Immunol. 2000 Nov 15;165(10):5387-91. doi: 10.4049/jimmunol.165.10.5387.
Although they are known for their capacity to kill infected cells, Ag-specific CD8(+) T cells elaborate other effector mechanisms, including TNF and IFN-gamma, that contribute to defense against infection. Ag-specific CD8(+) T cells rapidly turn ON and turn OFF IFN-gamma production in direct response to Ag contact, presumably to minimize the potential immunopathology that could result from inappropriate secretion of this inflammatory mediator. In this study, we show, using in vitro propagated and directly ex vivo-analyzed Ag-specific CD8(+) T cells, that in contrast to Ag-dependent ON/OFF cycling of IFN-gamma production, the cessation of TNF production by the same IFN-gamma producing cells is rapid and Ag independent.
尽管Ag特异性CD8(+) T细胞以其杀伤被感染细胞的能力而闻名，但它们还会发挥其他效应机制，包括肿瘤坏死因子（TNF）和干扰素-γ（IFN-γ），这些机制有助于抵御感染。Ag特异性CD8(+) T细胞在直接接触抗原后会迅速开启和关闭IFN-γ的产生，推测这是为了尽量减少因这种炎症介质分泌不当而可能导致的潜在免疫病理反应。在本研究中，我们使用体外增殖并直接进行离体分析的Ag特异性CD8(+) T细胞表明，与IFN-γ产生的抗原依赖性开启/关闭循环不同，相同的产生IFN-γ的细胞停止产生TNF的过程迅速且不依赖抗原。
