Marrack P, Kappler J W
J Exp Med. 1979 Mar 1;149(3):780-5. doi: 10.1084/jem.149.3.780.
We examined the expression of (TG)-A--L specific Ir genes in helper T cells using T cells from low responder leads to (B10, high responder x low responder) F1 chimeric mice. In this paper, the low responder strain studied was B10.M, H-2f. B10.M T cells from these chimeric animals do not help anti-TNP-(TG)-A--L responses, even though they have matured in a high responder thymus and been primed and challenged with antigen on high responder Mphi and B cells. These findings indicate that in the H-2f haplotype an Ir-gene controlling anti-(TG)-A--L activity is expressed in helper T cells. The findings are in contrast to those we have obtained and previously reported with T cells of another low responder haplotype, H-2a. Taken together with our previous findings that (TG)-A--L specific Ir genes are expressed by B cells and Mphi of both the H-2a and H-2f haplotypes, the results indicate two sites of action for Ir genes, and suggest two different gene products acting at different stages of the response, both of which are defective in H-2f cells, and only one of which is defective in H-2a cells.
我们使用来自低反应性亲代(B10,高反应性×低反应性)F1嵌合小鼠的T细胞,检测了辅助性T细胞中(TG)-A--L特异性Ir基因的表达。在本文中,所研究的低反应性品系是B10.M,H-2f。来自这些嵌合动物的B10.M T细胞不能辅助抗TNP-(TG)-A--L反应,即使它们在高反应性胸腺中成熟,并在高反应性巨噬细胞和B细胞上用抗原进行了致敏和激发。这些发现表明,在H-2f单倍型中,控制抗(TG)-A--L活性的Ir基因在辅助性T细胞中表达。这些发现与我们用另一种低反应性单倍型H-2a的T细胞所获得并先前报道的结果形成对比。结合我们先前的发现,即(TG)-A--L特异性Ir基因由H-2a和H-2f单倍型的B细胞和巨噬细胞表达,结果表明Ir基因有两个作用位点,并提示两种不同的基因产物在反应的不同阶段起作用,这两种产物在H-2f细胞中均有缺陷,而在H-2a细胞中只有一种有缺陷。