Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Type

Journal article

Journal

Immunity

Publication Date

07/1996

Volume

5

Pages

41 - 52

Keywords

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