The equilibrium of signaling through activating and inhibitory receptors dictates whether a given NK cell will execute cellular cytotoxicity. In this issue of the JCI, Kamiya et al. describe a novel approach to efficiently inhibiting surface expression of the inhibitory receptor CD94/NK group 2 member A (NKG2A) through retention of the protein in the endoplasmic reticulum. In adoptive transfer experiments into tumor-bearing immunodeficient mice, NKG2Anull NK cells were significantly more effective at eliminating HLA-E–expressing tumor cells than NKG2A+ NK cells. This study provides proof of concept for a new immunotherapeutic approach using NKG2Anull NK cells.
Bibliographical noteFunding Information:
We would like to acknowledge the following sources of NIH funding: K99/R00 HL123638 (to FC) and P01 CA111412, P01 CA65493, and R35 CA197292 (to JSM).
PubMed: MeSH publication types
- Journal Article
- Research Support, N.I.H., Extramural