Anti-Mouse NKG2A/C/E (20D5) In Vivo Antibody - Low Endotoxin (ICH1171-100mg)

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This product is the rat anti-mouse NKG2A/C/E monoclonal antibody, clone 20D5 (rat IgG2a isotype), supplied in an in-vivo-ready, low-endotoxin format for research use only. Clone 20D5 recognizes an epitope shared across the mouse CD94-associated NKG2 family members NKG2A, NKG2C and NKG2E (CD159a/c/e), receptors expressed predominantly on natural killer (NK) cells and subsets of activated CD8 T cells. Because 20D5 binds the shared NKG2 ectodomain, it is widely used to interrogate and modulate NKG2A-mediated inhibitory signaling in NK-cell biology, tumor immunology, and viral immunity. The rat IgG2a backbone and validated cross-reactivity within the mouse NKG2A/C/E family make it well suited to functional flow-cytometry phenotyping and in-vivo receptor-blockade experiments in immunocompetent mouse models. ichorbio supplies this clone at low endotoxin (research grade <1 EU/mg; ultra-low <0.5 EU/mg) and in bulk milligram-to-gram quantities to support repeat-dosing in-vivo study designs, giving researchers a consistent, affordable reagent for NK-cell checkpoint and adoptive-transfer work. All material is intended as a research reagent for the customer to validate in their own system. NKG2A, NKG2C and NKG2E are C-type lectin-like receptors that pair covalently with CD94 to form heterodimers on NK cells and some activated CD8 T cells. In mice these receptors recognize the non-classical MHC class I molecule Qa-1b (the functional homolog of human HLA-E), which presents peptides derived from the leader sequences of classical MHC class I. The CD94/NKG2A heterodimer is inhibitory: engagement of Qa-1b delivers an ITIM-mediated "off" signal that restrains NK-cell cytotoxicity and cytokine output, contributing to missing-self recognition and self-tolerance. In contrast, CD94/NKG2C and NKG2E are activating receptors that signal through DAP12. Because NKG2A functions as an NK-cell checkpoint that tumors and virally infected cells can exploit by upregulating Qa-1b/HLA-E, blocking this inhibitory axis is of substantial interest for enhancing NK- and T-cell-mediated immunity.

NK cells and NK T cells from C57BL/6 mouse