Dunlop M B, Blanden R V
J Exp Med. 1977 May 1;145(5):1131-43. doi: 10.1084/jem.145.5.1131.
The cytotoxic T-cell response to lymphocytic choriomeningitis (LCM) virus infection was suppressed either in vitro or in vivo by addition of a high level of syngeneic virus-infected cells or syngeneic cells from congenital LCM virus carriers to the environment of the responding cells. This effect was not duplicated by formaldehyde-fixed carrier cells, nor could it be accounted for by 'cold' target competition by carrier cells at the level of the cytotoxicity assay. Conversely, suppression was produced in vivo by water-lysed, ultrasonically treated carrier cell suspensions, or by a large dose of LCM virus equivalent to that contained in the carrier cells. Thus a high level of infectious virus was a common factor in all observed examples of suppression. Based upon this, the following hypothesis, a form of 'forbidden clone deletion,' was proposed to account for virus-specific cytotoxic T-cell tolerance in LCM virus congenital carriers, or in high dose suppression. A high level of virus in lymphoid tissues, while not cytopathic per se, may result in infection of all or most T cells; this then may lead to deletion either via 'suicide' of individual, infected, cytotoxic T cells with receptors specific for virus-induced antigenic patterns on their own surface membranes, or by mutual lysis of two adjacent T cells.
通过向反应细胞环境中添加高水平的同基因病毒感染细胞或先天性淋巴细胞性脉络丛脑膜炎(LCM)病毒携带者的同基因细胞,对LCM病毒感染的细胞毒性T细胞反应在体外或体内均受到抑制。甲醛固定的载体细胞不会产生这种效果,细胞毒性测定水平上的载体细胞“冷”靶竞争也无法解释这种现象。相反,体内抑制作用是由水溶、超声处理的载体细胞悬液或相当于载体细胞所含剂量的大剂量LCM病毒产生的。因此,高水平的感染性病毒是所有观察到的抑制实例中的共同因素。基于此,提出了以下假说,即一种“禁忌克隆缺失”形式,以解释LCM病毒先天性携带者或高剂量抑制中的病毒特异性细胞毒性T细胞耐受性。淋巴组织中高水平的病毒本身虽无细胞病变作用,但可能导致所有或大多数T细胞被感染;这进而可能通过以下方式导致缺失:要么是具有针对自身表面膜上病毒诱导抗原模式的受体的单个被感染细胞毒性T细胞“自杀”,要么是两个相邻T细胞相互裂解。