CD4 and CD8 accessory molecules function through interactions with major histocompatibility complex molecules which are not directly associated with the T cell receptor-antigen complex.

摘要: Both the subset-specific, CD4 and CD8 T cell accessory molecules antigen-specific receptor (TcR) interact with major histocompatibility complex (MHC) class I II on surface of antigen-presenting cells. We analyzed whether CD4/CD8 exert their function through binding same MHC which participate in TcR-antigen-MHC complex. utilized a CD4-, CD8-, I-allospecific hybridoma functionally manifests both cytotoxic lymphocyte (CTL) helper1 (Th1) phenotypes, rendered it bispecific by transfecting genes encoding either II-restricted, 2,4,6-trinitrophenyl (TNP)-I-Ad-specific TcR or non-MHC-restricted chimeric TcR, composed variable part an anti-TNP antibody. Expression transgenes these hybridomas enhanced augmented reactivity towards appropriate target cells regardless type TcR-MHC interaction. Thus, I-specific responses could be CD4-class interactions, II-restricted CD8-class interactions. Furthermore, also potentiated TNP-specific is unrestricted. The facilitated interleukin 2 (IL2) production cytolytic activity shortening activation time rendering responsive to lower antigenic stimuli. degree correlated level molecule expression was not related effector mediated Anti-CD4 -CD8 antibodies completely inhibited transfectants expressing corresponding molecule, Such blocked direct stimulation provided anti-T3/Ti lectins, but inhibit agents that bypass such as phorbol 12-myristate 13-acetate plus ionophore. Taken together, studies demonstrate CD8/CD4 can interactions are directly associated TcR-Ag-MHC complex, this effect TcR-mediated triggering at early stage signaling process mechanism assigned subsets.