Cluster of differentiation in cytotoxic T cell

Most cytotoxic T cells express T-cell receptors (TCRs) that can recognize a specific antigen. An antigen is a molecule capable of stimulating an immune response, and is often produced by cancer cells or viruses. Two major forms of these polymorphic membrane-bound glycoproteins exist, MHC class I and class II molecules. Class I and class II molecules interact with different coreceptors on the T cells, that is, CD8 and CD4, respectively. If the TCR is specific for that antigen, it binds to the complex of the class I MHC molecule and the antigen, and the T cell destroys the cell.
In order for the TCR to bind to the class I MHC molecule, the former must be accompanied by a glycoprotein called CD8, which binds to the constant portion of the class I MHC molecule. Therefore, these T cells are called CD8+ T cells. The affinity between CD8 and the MHC molecule keeps the TC cell and the target cell bound closely together during antigen-specific activation.

CD8+ T cells are critical for controlling many viral infections and are central to vaccine-induced antiviral immunity. During the primary response to an acute viral infection, naive CD8+ T cells are driven in a predominantly Ag-specific manner to become effector T cells. After resolving the infection, the majority of virus-specific T cells die by activation-induced cell death, but a population of memory T cells is stably maintained for life; up to 2 years in mice and 35–50 years in humans. Several murine surface markers distinguish naive T cells from activated/memory T cells, including CD11a, CD11b, CD44, CD62L, and peanut lectin agglutinin, but there are currently no surface markers that can be used to distinguish activated T cells from memory T cells in normal mice.