Dendritic cell-Natural Killer cell surface receptors (DC-NK receptors)

Dendritic cell-Natural Killer (DC-NK) cell surface receptors are a collective group of molecules that facilitate the essential bidirectional communication between DCs and NK cells, bridging innate and adaptive immunity [5]. This crosstalk involves a variety of activating receptors on NK cells, such as NKp30, NKp46, and NKG2D, which interact with specific ligands on DCs like BAG6 and MICA/B to trigger NK cell activation and cytokine release [7, 12]. Conversely, NK cells influence DC maturation and "editing" (the elimination of immature DCs) through receptors like NKp30 and the secretion of TNF-alpha and IFN-gamma [10, 11]. In many diseases, particularly cancer, this interaction is compromised by the tumor microenvironment, which may downregulate activating ligands or exploit inhibitory pathways like the NKG2A/HLA-E axis to evade immune detection [6, 15]. Consequently, these receptors have become significant therapeutic targets, with drugs like Monalizumab designed to block inhibitory signals and restore the synergistic activation of both cell types [15]. Enhancing DC-NK crosstalk is a promising strategy to improve the efficacy of cancer vaccines and other immunotherapies by ensuring robust antigen presentation and potent cytotoxic responses [12, 13]. The regulation of these receptors is also critical in viral infections and inflammatory conditions where the balance of NK-DC signals determines the strength and quality of the immune response [4, 8].

Other names

NK-DC crosstalk receptorsDC-NK interaction receptorsNatural cytotoxicity receptorsNCRs

Modulation of the bidirectional crosstalk between dendritic cells and natural killer cells to enhance anti-tumor or anti-viral immunity through checkpoint inhibition or receptor activation.