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Title: CD4+ proliferative T-cell clones reactive to autologous Epstein-Barr virus-transformed B cells (EBV-LCL) can be restricted by HLA class I molecules. Author: Chen BP, DeMars R, Hank JA, Sondel PM. Journal: Cell Immunol; 1988 Sep; 115(2):363-72. PubMed ID: 2842068. Abstract: In this study, we show that an HLA-loss variant, EBV-LCL .180, which lacks HLA-DR, DP, DQ and B determinants but expresses HLA-A and C molecules, can activate autologous proliferative T cells which recognize EBV-LCL antigens (or LYDMA). T-cell clones isolated from bulk culture (A.180) of T cell primed with autologous variant .180 when tested for their proliferative reactivity to .180 and three autologous class I-loss variants, each lacking specific class I determinants, showed requirement for class I HLA molecules. Clones A.180.Cl and A.180.F3D respond to the A2+, B-null, C+ mutant .53, but not to the A-null, B5+, C+ mutant .144, or the A-null, B-null, C+ mutant .184, indicating that these clones are restricted by an HLA-A2 determinant. These proliferative T-cell clones express the CD4 marker and are noncytotoxic, even in the presence of concanavalin A (Con A) lectin. In coculture experiments, A.180.Cl was further shown to provide lymphokine "help" for EBV-LCL-specific, autologous cytotoxic T-cell clones. These results suggest the repertoire of HLA determinants employed by EBV-LCL-specific proliferative T cells, in addition to the previously shown HLA-DR, DP, and DQ determinants, also includes class I molecules.[Abstract] [Full Text] [Related] [New Search]