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Current models suggest that T cells that receive only signal-1 through antigenic stimulation of the T cell receptor (TCR) become anergic, but will mount an immune response when a costimulatory signal-2 is provided. Using mice deficient for an important costimulatory molecule, CD28, we show that a transient signal-1 alone, either through infection with an abortively replicating virus, or through injection of viral peptide, anergizes CD8+ T cells, demonstrating the biological relevance of T cell anergy in vivo. However, in the absence of CD28, continued presence of signal-1 alone, either through prolonged viral replication or repeated injection of peptide, prevents the induction of anergy and generates a functional T cell response in vivo.


Journal article



Publication Date





41 - 52


Animals, Antigens, Viral, CD28 Antigens, Clonal Deletion, Cytotoxicity, Immunologic, Dose-Response Relationship, Immunologic, Immune Tolerance, Lymphocyte Activation, Lymphocytic choriomeningitis virus, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Mutant Strains, Receptors, Antigen, T-Cell, T-Lymphocytes, Cytotoxic, Virus Replication