Nabavi N, Freeman G J, Gault A, Godfrey D, Nadler L M, Glimcher L H
Department of Immunopharmacology, Roche Research Center, Nutley, New Jersey 07110.
Nature. 1992 Nov 19;360(6401):266-8. doi: 10.1038/360266a0.
Class II major histocompatibility complex (MHC) molecules function as antigen-presenting elements as well as signal transducers on B lymphocytes. We previously reported that a B lymphoma cell transfectant, 5C2, expressing genetically engineered I-Ak molecules with truncated cytoplasmic domains was severely impaired in both antigen presentation and in anti-Ia-induced intracytoplasmic signalling. These two functions could be restored by preculturing 5C2 cells with cyclic AMP analogues. Here we demonstrate that impaired signal transduction by truncated class II molecules results in a deficiency in induction of the newly defined B-cell accessory molecule B7 (ref. 8), which can be reversed by restoration of B7 expression. These data imply that contact of the T-cell antigen receptor with MHC/antigen ligand results in signal transmission through the class II cytoplasmic domain. This signal, which can be mimicked by dibutyryl cAMP, induces expression of B7, resulting in effective antigen presentation. The fact that crosslinking of surface class II MHC also induces B7 expression on normal resting human B cells supports this contention.
II类主要组织相容性复合体（MHC）分子在B淋巴细胞上作为抗原呈递元件以及信号转导分子发挥作用。我们之前报道过，一个表达带有截短细胞质结构域的基因工程改造的I-Ak分子的B淋巴瘤细胞转染体5C2，在抗原呈递和抗Ia诱导的胞内信号传导方面均严重受损。通过用环磷酸腺苷类似物预培养5C2细胞，这两种功能可以恢复。在此我们证明，截短的II类分子导致的信号转导受损会致使新定义的B细胞辅助分子B7（参考文献8）诱导不足，而B7表达的恢复可以逆转这种情况。这些数据表明，T细胞抗原受体与MHC/抗原配体的接触会导致信号通过II类细胞质结构域进行传递。这个可以被二丁酰环磷腺苷模仿的信号会诱导B7的表达，从而导致有效的抗原呈递。表面II类MHC的交联也会在正常静息人B细胞上诱导B7表达，这一事实支持了这一论点。
