Integral membrane glycoprotein that plays an essential role in the immune response and serves multiple functions in responses against both external and internal offenses. In T-cells, functions primarily as a coreceptor for MHC class I molecule:peptide complex. The antigens presented by class I peptides are derived from cytosolic proteins while class II derived from extracellular proteins. Interacts simultaneously with the T-cell receptor (TCR) and the MHC class I proteins presented by antigen presenting cells (APCs). In turn, recruits the Src kinase LCK to the vicinity of the TCR-CD3 complex. LCK then initiates different intracellular signaling pathways by phosphorylating various substrates ultimately leading to lymphokine production, motility, adhesion and activation of cytotoxic T-lymphocytes (CTLs). This mechanism enables CTLs to recognize and eliminate infected cells and tumor cells. In NK-cells, the presence of CD8A homodimers at the cell surface provides a survival mechanism allowing conjugation and lysis of multiple target cells. CD8A homodimer molecules also promote the survival and differentiation of activated lymphocytes into memory CD8 T-cells. Forms disulfide-linked heterodimers with CD8B at the cell surface. Forms also homodimers in several cell types including NK-cells or peripheral blood T-lymphocytes. Interacts with the MHC class I HLA-A/B2M dimer. Interacts with LCK in a zinc-dependent manner. Cd8a localizes to lipid rafts only when associated with its partner Cd8b. A number of isoforms are produced. Alternative splicing involves excision of the transmembrane or cytoplasmic domains. Palmitoylated, but association with CD8B seems to be more important for the enrichment of CdD8A in lipid rafts. Phosphorylated in cytotoxic T-lymphocytes (CTLs) following activation. Cd8a-deficient mice prevent the development of class I MHC restricted cytotoxic T-cells. However, maturation of class II MHC restricted T-helper cells seems to be unaffected by the absence of Cd8a.