Vidović D, Klein J, Nagy Z A
J Immunol. 1985 Jun;134(6):3563-8.
The proliferative T cell response of inbred mouse strains to the random copolymer poly(Glu50Tyr50) (GT) was found to fall into two categories. Some strains responded only marginally (delta cpm values less than 10,000 and stimulation indices less than 3), whereas other strains mounted a substantial response (delta cpm 10,000 to 80,000, SI 3 to 30). The response is controlled by the A alpha and A beta loci of the major histocompatibility complex (MHC), as well as by genes not linked to the MHC. Because the response is selectively inhibited by monoclonal antibodies specific for the A alpha A beta molecule, we assume that its control by A loci is manifested as an A-restriction of the participating T (Ly-1high, Ly-2-) cells. It is of interest that the responsiveness is recessive in F1 hybrids of responder and nonresponder strains that are H-2-identical, but differ at their genetic background. Nonresponsiveness of these F1 mice is caused neither by a defect of antigen presentation, nor the result of immune suppression on priming or at the effector phase of the response. It is most likely the consequence of clonal deletion during the establishment of self-tolerance.
近交系小鼠品系对随机共聚物聚(谷氨酸50酪氨酸50)(GT)的增殖性T细胞反应分为两类。一些品系反应微弱(δcpm值小于10,000,刺激指数小于3),而其他品系则有显著反应(δcpm为10,000至80,000,SI为3至30)。该反应受主要组织相容性复合体(MHC)的Aα和Aβ基因座以及与MHC不连锁的基因控制。由于该反应被针对AαAβ分子的单克隆抗体选择性抑制,我们推测其由A基因座控制表现为参与的T(Ly-1高,Ly-2-)细胞的A限制性。有趣的是,在H-2相同但遗传背景不同的反应品系和无反应品系的F1杂种中,反应性是隐性的。这些F1小鼠的无反应性既不是由抗原呈递缺陷引起的,也不是免疫抑制在反应的启动阶段或效应阶段的结果。这很可能是在建立自身耐受性期间克隆缺失的结果。