CD8a Monoclonal Antibody (OKT8 (OKT-8)), Functional Grade, eBioscience™, Invitrogen™

Description

• The OKT8 MAb reacts with the human CD8a molecule, an approximately 32-34 kDa cell surface receptor expressed either as a heterodimer with the CD8 beta chain (CD8 alpha beta) or as a homodimer (CD8 alphaalpha)
• A majority of thymocytes and a subpopulation of mature T cells and NK cells express CD8a
• CD8 binds to MHC class I and through its association with protein tyrosine kinase p56lck plays a role in T-cell development and activation of mature T cells
• Preliminary testing indicates that OKT8 and two other mouse anti-human CD8 antibodies (clone RPA-T8, Cat
• No.14-0088 and clone HIT8a, Cat
• No.14-0089) do not compete with each other for binding to human peripheral blood leukocytes by flow cytometric analysis, suggesting that they do not bind to similar epitopes or block each other by steric hindrance
• Cluster of differentiation 8 (CD8), a type I transmembrane glycoprotein of the immunoglobulin family of receptors, plays an integral role in signal transduction, and T cell differentiation and activation
• CD8 is predominantly expressed on T cells as a disulfide-linked heterodimer of CD8alpha and CD8beta, where it functions as a co-receptor, along with T cell receptor (TCR), for major histocompatibilty complex class I (MHC-I) molecules; whereas its counterpart, CD4, acts as a co-receptor for MHC-II molecules
• CD8 exists on the cell surface, where the CD8alpha chain is essential for binding to MHC-I
• CD8 is also expressed on a subset of T cells, NK cells, monocytes and dendritic cells as disulfide-linked homodimers of CD8alpha
• Ligation of MHC-I/peptide complexes presented by antigen-presenting cells (APCs), triggers the recruitment of lymphocyte-specific protein tyrosine kinase (Lck), which leads to lymphokine production, motility and cytotoxic T lymphocyte (CTL) activation
• Once activated, CTLs play a crucial role in the clearance of pathogens and tumor cells
• Differentiation of naive CD8+ T cells into CTLs is strongly enhanced by IL-2, IL-12 and TGF-beta1.