Hämmerling G, McDevitt H O
J Exp Med. 1974 Nov 1;140(5):1180-8. doi: 10.1084/jem.140.5.1180.
(125)I-A--L-binding T cells have been studied in mice whose ability to mount an immune response to (T,G)-A--L is under control of the H-2-linked Ir-1A gene. Nonimmunized high and low responder mice have approximately the same frequency of T-ABC. Following immunization, T-ABC proliferated only in high responders, but not in low responders, indicating expression of Ir-1A in T cells. When, for comparison, [(125)I]arsanyl-mouse serum albumin binding B and T cells were investigated in mice whose antibody response to the hapten arsanyl is controlled by an allotype-linked Ir gene, it was found that following immunization the number of B-ABC increased only in high responders. In contrast, T-ABC proliferated to the same extent in both high and low responders, suggesting exclusive expression of the allotype-linked Ir gene in the B-cell line. Preliminary studies indicate that anti-Ia sera inhibit neither B-ABC nor T-ABC.
已经在对(T,G)-A-L产生免疫应答的能力受H-2连锁的Ir-1A基因控制的小鼠中研究了[(125)I](T,G)-A-L结合T细胞。未免疫的高应答和低应答小鼠具有大致相同频率的T-ABC。免疫后,T-ABC仅在高应答者中增殖,而在低应答者中不增殖,表明Ir-1A在T细胞中表达。作为比较,当在对半抗原砷酰基的抗体应答受同种异型连锁的Ir基因控制的小鼠中研究[(125)I]砷酰基-小鼠血清白蛋白结合B细胞和T细胞时,发现免疫后B-ABC的数量仅在高应答者中增加。相反,T-ABC在高应答者和低应答者中增殖程度相同,表明同种异型连锁的Ir基因仅在B细胞系中表达。初步研究表明,抗Ia血清既不抑制B-ABC也不抑制T-ABC。