Sunday M E, Benacerraf B, Dorf M E
J Exp Med. 1981 Apr 1;153(4):811-22. doi: 10.1084/jem.153.4.811.
In the current study, we examine the mechanism of suppression of cutaneous sensitivity (CS) responses to 4-hydroxy-3-nitrophenyl acetyl succinimide ester. Intravenous administration of haptenated syngeneic spleen cells induces a state of hapten-specific tolerance involving I-J bearing suppressor T cells that function at either the induction phase or the effector phase of the CS response. The effective phase suppressor cells (Tse) are genetically restricted by both Igh and H-2 region genes. However, a third cell population is also required in he immune lymphocyte population for immune suppression. This third cell population, termed Ts3, is an I-J+, cyclophosphamide-sensitive T cell, as shown by reconstitution experiments. Further, the Tse-Ts3 interaction is restricted by genes in he H-2 and Igh gene complexes. The results are discussed with respect to the pathway of cellular interactions leading to immuno suppression.
在当前研究中,我们研究了对4-羟基-3-硝基苯基乙酰琥珀酰亚胺酯的皮肤敏感性(CS)反应的抑制机制。静脉注射半抗原化的同基因脾细胞可诱导一种半抗原特异性耐受状态,涉及带有I-J的抑制性T细胞,这些细胞在CS反应的诱导阶段或效应阶段发挥作用。有效的阶段抑制细胞(Tse)在遗传上受Igh和H-2区域基因的限制。然而,免疫淋巴细胞群体中还需要第三种细胞群体来进行免疫抑制。如重建实验所示,这种第三种细胞群体称为Ts3,是一种I-J +、对环磷酰胺敏感的T细胞。此外,Tse-Ts3相互作用受H-2和Igh基因复合物中的基因限制。我们就导致免疫抑制的细胞相互作用途径对结果进行了讨论。