Dick T, Staege M S, Reichmann G, Reske-Kunz A B
Institute for Immunology, Johannes Gutenberg University, Mainz, Germany.
J Immunol. 1993 Apr 1;150(7):2575-83.
10BK.1 T clone cells of (B10 x B10.BR)F1 genotype specifically react to peptides of OVA, frequently encountered in OVA preparations, and to the synthetic peptide OVA257-264 in an H-2Kb-restricted manner; the T clone cells produce lymphokines and proliferate in the absence of added APC, suggesting self-presentation of the Ag by the T cells. In accordance with their CD8+ CD4- phenotype 10BK.1 cells exhibit cytotoxic capacity. When the target cells were pretreated with OVA257-264 only cells bearing H-2Kb molecules were lysed. However, when the relevant OVA peptide was present during the 4-h 51Cr release assay 10BK.1 cells lysed target cells expressing H-2Kb molecules as well as target cells lacking H-2Kb elements. Likewise, 10BK.1 cells pretreated with OVA257-264 for 1 h and washed extensively to remove residual Ag were able to kill syngeneic and allogeneic target cells. Killing of allogeneic targets in the presence of Ag was inhibited by antibodies directed at H-2Kb. Allogeneic target cells were not killed when 10BK.1 cells were stimulated by peptide-pulsed syngeneic cells. Triggering of the TCR/CD3 complex of 10BK.1 cells was involved during the activation phase but not during the lytic phase. IL-2 did not participate in the MHC-unrestricted killing event. To explain the observed MHC-unrestricted cytotoxicity of 10BK.1 cells, the following model is proposed. In an initial step 10BK.1 cells present the relevant OVA peptide to one another in a H-2Kb-restricted fashion. The cells are thereby triggered to mobilize the lytic machinery. In a second step sensitized 10BK.1 cells lyse allogeneic target cells. Thus, the MHC-unrestricted cytotoxicity can be dissected into an MHC-restricted phase of 10BK.1 cell activation and an MHC-unrestricted lytic phase. Cytotoxic T cells with Ag self-presentation functions may account for tissue damage during bacterial infections.
10BK.1（B10×B10.BR）F1基因型的T克隆细胞对卵清蛋白（OVA）制剂中常见的OVA肽以及合成肽OVA257 - 264以H - 2Kb限制性方式特异性反应；这些T克隆细胞在不添加抗原呈递细胞（APC）的情况下产生淋巴因子并增殖，提示T细胞自身呈递抗原。根据其CD8 + CD4 - 表型，10BK.1细胞具有细胞毒性能力。当用OVA257 - 264预处理靶细胞时，只有携带H - 2Kb分子的细胞被裂解。然而，当在4小时51Cr释放试验期间存在相关的OVA肽时，10BK.1细胞裂解表达H - 2Kb分子的靶细胞以及缺乏H - 2Kb元件的靶细胞。同样，用OVA257 - 264预处理1小时并广泛洗涤以去除残留抗原的10BK.1细胞能够杀死同基因和异基因靶细胞。在抗原存在下对异基因靶细胞的杀伤被针对H - 2Kb的抗体抑制。当10BK.1细胞被肽脉冲的同基因细胞刺激时，异基因靶细胞未被杀死。10BK.1细胞的TCR/CD3复合物的触发在激活阶段起作用，但在裂解阶段不起作用。白细胞介素 - 2不参与MHC非限制性杀伤事件。为了解释观察到的10BK.1细胞的MHC非限制性细胞毒性，提出了以下模型。在第一步中，10BK.1细胞以H - 2Kb限制性方式将相关的OVA肽相互呈递。细胞因此被触发以启动裂解机制。在第二步中，致敏的10BK.1细胞裂解异基因靶细胞。因此，MHC非限制性细胞毒性可分为10BK.1细胞激活的MHC限制性阶段和MHC非限制性裂解阶段。具有抗原自我呈递功能的细胞毒性T细胞可能是细菌感染期间组织损伤的原因。
