Stukart M J, Boes J, Melief C J
J Immunol. 1984 Jul;133(1):28-32.
We have studied the effect of mutations in H-2Kb on recognition of Moloney virus antigens by Kb-restricted Moloney virus-specific cytotoxic T lymphocytes (CTL) generated from H-2Db-mutant B6.C-H- 2bm13 ( bm13 ) mice. On the basis of the bm13 virus-specific recognition pattern of a series of Kb-mutant virus-infected (V+) cells, these Kb mutants could be divided into two groups that either shared the relevant H-2K restriction specificities with H-2Kb ( bm3 , bm5 , bm6 , and bm11 ) or lacked them completely (bm1) and/or almost completely ( bm8 ). In the study presented in this report, we concentrated on the alloreactive CTL included in the repertoire of bm13 Moloney-specific CTL. These CTL lysed noninfected (V-) allogeneic target cells of many H-2 types, including all Kb-mutant cells tested (bm1, bm3 , bm5 , bm6 , bm8 , and bm11 ). Recognition of V- cells of two Kb mutants, bm3 and bm11 , which share a common amino acid substitution at position 77 of the H-2K molecule with an additional change at position 89 in bm3 , was compared with recognition of the other Kb-mutant V- target cells in cold target inhibition studies. These studies showed that bm3 and bm11 cells share a determinant or determinants on the H-2K molecule recognized by alloreactive CTL among the Moloney virus-specific CTL population not present on the other Kb-mutant cells; lysis of both target cells was inhibited only by bm3 and bm11 V- cells. On the other hand, lysis of bm3 V+ target cells by bm13 virus-specific CTL was inhibited by all Kb-mutant V+ cells ( bm3 , bm5 , bm6 , and bm11 ) that were killed virus specifically by bm13 CTL. Thus, common determinants on the H-2K molecule of these Kb-mutant V+ cells are recognized by Kb-restricted Moloney virus-specific CTL. From the difference in inhibition pattern of the lytic reaction against bm3 V+ vs bm3 V- cells, we conclude that determinants on the same H-2K molecule recognized by Moloney virus-specific CTL and allocross -reactive effector cells included in the Moloney virus-specific population are not identical.
我们研究了H-2Kb突变对来自H-2Db突变的B6.C-H-2bm13(bm13)小鼠产生的Kb限制性莫洛尼病毒特异性细胞毒性T淋巴细胞(CTL)识别莫洛尼病毒抗原的影响。根据一系列Kb突变病毒感染(V+)细胞的bm13病毒特异性识别模式,这些Kb突变体可分为两组,一组与H-2Kb共享相关的H-2K限制性特异性(bm3、bm5、bm6和bm11),另一组则完全缺乏(bm1)和/或几乎完全缺乏(bm8)。在本报告中的研究中,我们集中研究了bm13莫洛尼特异性CTL库中包含的同种反应性CTL。这些CTL可裂解许多H-2类型的未感染(V-)同种异体靶细胞,包括所有测试的Kb突变细胞(bm1、bm3、bm5、bm6、bm8和bm11)。在冷靶抑制研究中,比较了两个Kb突变体bm3和bm11的V-细胞的识别情况,这两个突变体在H-2K分子的第77位氨基酸有共同取代,bm3在第89位还有额外变化,与其他Kb突变体V-靶细胞的识别情况进行比较。这些研究表明,bm3和bm11细胞在H-2K分子上共享一个或多个决定簇,这些决定簇可被莫洛尼病毒特异性CTL群体中的同种反应性CTL识别,而其他Kb突变细胞上不存在这些决定簇;只有bm3和bm11的V-细胞可抑制两种靶细胞的裂解。另一方面,bm13病毒特异性CTL对bm3 V+靶细胞的裂解可被所有被bm13 CTL特异性杀伤病毒的Kb突变V+细胞(bm3、bm5、bm6和bm11)抑制。因此,这些Kb突变V+细胞的H-2K分子上的共同决定簇可被Kb限制性莫洛尼病毒特异性CTL识别。根据针对bm3 V+与bm3 V-细胞的裂解反应抑制模式的差异,我们得出结论,莫洛尼病毒特异性CTL和莫洛尼病毒特异性群体中包含的同种交叉反应效应细胞识别的同一H-2K分子上的决定簇并不相同。