Levy R B, Shearer G M
J Exp Med. 1979 Jun 1;149(6):1379-92. doi: 10.1084/jem.149.6.1379.
Spleen cells from H-2b,k,d C57Bl/10 congenic mice were sensitized in vitro to trinitrobenzenesulfonate (TNBS)-modified autologous spleen cells. Cold target competition studies at the lytic phase demonstrated three distinct patterns of cytotoxic responsiveness: (a) H-2b spleen cells generated approximately equivalent CTL responses against Kb and Db modified self products, (b) H-2d spleen cells generated preferential responses against Dd modified self products, and (c) H-2k spleen cells generated cytotoxic responses which could only be detected against Kk self products in association with TNP. F1 spleen cells were sensitized against autologous TNBS-treated cells. The results showed that, although H-2b parental cells generated approximately equivalent Kb-TNP- and Db-TNP-specific CTL, the presence of the H-2b haplotype did not result in the generation of (a) Dk-TNP CTL response by (H-2b x H-2k) spleen cells, nor (b) a Db CTL response by (H-2b x H-2a) F1 spleen cells. Additionally, (H-2d x H-2k) F1 cells failed to generate detectable Dd-TNP-specific CTL, although H-2d parental cells generated D-regional-specific CTL. The findings demonstrated that these F1 response patterns paralleled those of the H-2k and H-2a parents, i.e. weak or no D-region TNP-specific CTL were induced. Because (H-2d x H-2a) F1 responders stimulated with H-2d TNBS-treated cells did generate good Dd TNP responses, the results illustrated that the presence of responder genes was not sufficient to result in a D-region TNP CML. It is suggested that the absence of Kk alleles on the stimulating population is necessary for the generation of D-region TNP CTL in these F1's. Mechanisms which could account for these response patterns in parental F1 mice are discussed including immunodominance, suppression, T-cell response , and Ir-gene defects.
来自H-2b、k、d C57Bl/10同源小鼠的脾细胞在体外被三硝基苯磺酸（TNBS）修饰的自体脾细胞致敏。在裂解阶段进行的冷靶竞争研究显示出三种不同的细胞毒性反应模式：（a）H-2b脾细胞对Kb和Db修饰的自身产物产生大致相当的CTL反应；（b）H-2d脾细胞对Dd修饰的自身产物产生优先反应；（c）H-2k脾细胞产生的细胞毒性反应仅在与TNP相关时才能检测到针对Kk自身产物的反应。F1脾细胞被自体TNBS处理的细胞致敏。结果表明，尽管H-2b亲代细胞产生了大致相当的Kb-TNP和Db-TNP特异性CTL，但H-2b单倍型的存在并未导致（a）（H-2b×H-2k）脾细胞产生Dk-TNP CTL反应，也未导致（b）（H-2b×H-2a）F1脾细胞产生Db CTL反应。此外，（H-2d×H-2k）F1细胞未能产生可检测到的Dd-TNP特异性CTL，尽管H-2d亲代细胞产生了D区域特异性CTL。这些发现表明，这些F1反应模式与H-2k和H-2a亲代的反应模式相似，即诱导出的D区域TNP特异性CTL较弱或没有。因为用H-2d TNBS处理的细胞刺激的（H-2d×H-2a）F1反应细胞确实产生了良好的Dd TNP反应，所以结果表明反应基因的存在不足以导致D区域TNP CML。有人提出，刺激群体中不存在Kk等位基因是这些F1中产生D区域TNP CTL所必需的。讨论了可以解释亲代F1小鼠中这些反应模式的机制，包括免疫显性、抑制、T细胞反应和Ir基因缺陷。
