Enhancement of Suboptimal CD8 Cytotoxic T Cell Effector Function In Vivo Using Antigen-Specific CD80 Defective T Cells

摘要: T cell upregulation of B7 molecules CD80 and CD86 limits expansion in immunodeficient hosts; however, the relative roles separate from on CD4 versus CD8 cells a normal immune system are not clear. To address this question, we used parent-into-F1 (P→F1) murine model graft-versus-host disease transferred optimal suboptimal doses and/or knockout (KO) into F1 hosts. Enhanced elimination host B by KO was observed only at donor greatest for KO→F1 mice. Wild-type exhibited peak day 10; greater (day 10) proliferation effector CTL numbers wild-type→F1 Fas or programmed death-1 as homeostatic contraction days 12-14. Mixing studies demonstrated that maximal seen when both were deficient. These results indicate an important role Ag-activated limiting effectors part response. Our support further therapeutic targeting conditions characterized responses.