Saito S, Tadakuma T, Inoko H, Saito K
Department of Microbiology, Keio University School of Medicine, Tokyo, Japan.
Mol Immunol. 1988 Jun;25(6):569-75. doi: 10.1016/0161-5890(88)90079-x.
Our previous study demonstrated (1) that the presence of charged groups (amino and carboxyl groups) at the alpha-carbon of tyrosine is essential for activation of azobenzenearsonate-L-tryosine (ABA-L-Tyr specific T cells, and (2) that T cells recognizes ABA-L-Tyr in association with macromolecules on syngeneic spleen cells used as antigen presenting cells (APC). The present study was undertaken to confirm that the macromolecules on APC are Ia molecules, by using L cells transfected with A beta k and A alpha k genes as APC. I-Ak restricted ABA-L-Tyr specific cloned T cells, and T hybridoma cells were activated by ABA-L-Tyr in the presence of the L cell transfectants, of which expression of I-Ak molecules had been proven by specific binding of anti-I-Ak monoclonal antibody (MAb) 10.2.16 on the cell surface. The pattern of responses of I-Ak restricted ABA-L-Tyr specific T cells to various ABA-Tyr derivatives presented by the I-Ak expressing L cell transfectants was similar to the pattern obtained by using H-2k spleen cells as APC. Thus, ABA-L-Tyr and ABA-Tyr derivatives, which have both amino and carboxyl groups at the alpha-carbon of Tyr, presented by the L cell transfectants triggered good response of I-Ak restricted ABA-L-Tyr specific T cells. By contrast, ABA-Tyr derivatives, which lack the amino or carboxyl group, or both groups, at the alpha-carbon of Tyr, presented by the L cell transfectants could not activate the ABA-L-Tyr specific T cells at all. Furthermore, anti-I-Ak MAb, but not anti-I-Ek MAb, inhibited completely the response of I-Ak restricted ABA-L-Tyr specific T cells to ABA-L-Tyr presented by the L cell transfectants. These results indicate strongly that the macromolecules on APC which associate with ABA-L-Tyr are A beta k A alpha k gene products, i.e., I-Ak molecules.
（1）酪氨酸α-碳上带电荷基团（氨基和羧基）的存在对于偶氮苯胂酸-L-酪氨酸（ABA-L-Tyr特异性T细胞）的激活至关重要；（2）T细胞识别与用作抗原呈递细胞（APC）的同基因脾细胞上的大分子结合的ABA-L-Tyr。本研究旨在通过使用转染了Aβk和Aαk基因的L细胞作为APC来证实APC上的大分子是Ia分子。I-Ak限制的ABA-L-Tyr特异性克隆T细胞和T杂交瘤细胞在L细胞转染子存在的情况下被ABA-L-Tyr激活，其中I-Ak分子的表达已通过抗I-Ak单克隆抗体（MAb）10.2.16在细胞表面的特异性结合得到证实。I-Ak限制的ABA-L-Tyr特异性T细胞对由表达I-Ak的L细胞转染子呈递的各种ABA-Tyr衍生物的反应模式与使用H-2k脾细胞作为APC所获得的模式相似。因此，由L细胞转染子呈递的、在酪氨酸α-碳上同时具有氨基和羧基的ABA-L-Tyr和ABA-Tyr衍生物引发了I-Ak限制的ABA-L-Tyr特异性T细胞的良好反应。相比之下，由L细胞转染子呈递的、在酪氨酸α-碳上缺乏氨基或羧基或两者都缺乏的ABA-Tyr衍生物根本无法激活ABA-L-Tyr特异性T细胞。此外，抗I-Ak MAb完全抑制了I-Ak限制的ABA-L-Tyr特异性T细胞对由L细胞转染子呈递的ABA-L-Tyr的反应，而抗I-Ek MAb则没有。这些结果有力地表明，与ABA-L-Tyr结合的APC上的大分子是Aβk Aαk基因产物，即I-Ak分子。
