About InVivoMAb anti-mouse NKG2AB6 The 16A11 monoclonal antibody reacts with NKG2A from C57BL/6 mice, the antibody does not react with BALB/c or 129 mouse strains. NKG2A, also known as CD159a is a type II transmembrane glycoprotein which belongs to the killer cell lectin-like receptor (KLR) family. NKG2A is expressed on NK cells, NKT cells, and activated CD8 T cells. NKG2A forms a disulfide-bonded heterodimer with CD94 that can bind to non-classical MHC class I antigen Qa-1 on target cells and inhibit NK cell activation. InVivoMAb anti-mouse NKG2AB6 Specifications IsotypeMouse IgG2b, κ Recommended Isotype Control(s)InVivoMAb mouse IgG2b isotype control, unknown specificity Recommended Dilution BufferInVivoPure pH 7.0 Dilution Buffer ImmunogenC57BL/6 mouse CD94/NKG2A transfected CHO cells Reported ApplicationsFlow cytometry FormulationPBS, pH 7.0 Contains no stabilizers or preservatives Endotoxin<2EU/mg (<0.002EU/μg) Determined by LAL gel clotting assay Purity>95% Determined by SDS-PAGE Sterility0.2 μm filtration ProductionPurified from cell culture supernatant in an animal-free facility PurificationProtein A RRIDAB_2894759 Molecular Weight150 kDa StorageThe antibody solution should be stored at the stock concentration at 4°C. Do not freeze. Application ReferencesInVivoMAb anti-mouse NKG2AB6 (CLONE: 16A11)Vance, R. E., et al (2002). "Implications of CD94 deficiency and monoallelic NKG2A expression for natural killer cell development and repertoire formation" Proceedings of the National Academy of Sciences 99(2): 868-873. PubMedNatural killer (NK) cells are believed to achieve self-tolerance through the expression of self-MHC-specific inhibitory receptors, such as members of the Ly49 and CD94/NKG2 families. Individual Ly49 genes are stochastically expressed by NK subsets and are expressed in a monoallelic fashion, but little is known about the mechanisms underlying CD94/NKG2A expression. We show here that, like Ly49 genes, mouse Nkg2a is stochastically and monoallelically expressed. Thus, a single general mechanism controls expression of all known MHC-specific receptors by mouse NK cells. In addition, we find that DBA/2J mice are naturally CD94-deficient and do not express cell-surface CD94/NKG2A receptors, even on neonatal NK cells. Thus, self-tolerance of neonatal NK cells cannot be attributed to CD94/NKG2A expression. Taken together, the results lead to a reconsideration of current models of NK cell development and self-tolerance.
