Signalling through the MHC class II cytoplasmic domain is required for antigen presentation and induces B7 expression

Abstract

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 lym-phoma 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 signalling1-5. These two functions could be restored by preculturing 5C2 cells with cyclic AMP analogues 6,7. 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 reverse..