Commentary 10.1172/JCI128480

Setting traps for NKG2A gives NK cell immunotherapy a fighting chance

Frank Cichocki and Jeffrey S. Miller

Department of Medicine, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.

Address correspondence to: Jeffrey S. Miller, University of Minnesota, 420 Delaware Street SE, Minneapolis, Minnesota 55455, USA. Phone: 612.625.7409; Email: mille011@umn.edu.

Find articles by Cichocki, F. in: JCI | PubMed | Google Scholar

Department of Medicine, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.

Address correspondence to: Jeffrey S. Miller, University of Minnesota, 420 Delaware Street SE, Minneapolis, Minnesota 55455, USA. Phone: 612.625.7409; Email: mille011@umn.edu.

Find articles by Miller, J. in: JCI | PubMed | Google Scholar

First published April 15, 2019 - More info

J Clin Invest. https://doi.org/10.1172/JCI128480.
© 2019 American Society for Clinical Investigation
First published April 15, 2019 - Version history

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.

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