Disulphide-isomerase-enabled shedding of tumour-associated NKG2D ligands

Brett K. Kaiser, Daesong Yim, I-Ting Chow, Segundo Gonzalez, Zhenpeng Dai, Henning H. Mann, Roland K. Strong, Veronika Groh and Thomas Spies ()
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Brett K. Kaiser: Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, Washington 98109, USA
Daesong Yim: Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, Washington 98109, USA
I-Ting Chow: Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, Washington 98109, USA
Segundo Gonzalez: Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, Washington 98109, USA
Zhenpeng Dai: Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, Washington 98109, USA
Henning H. Mann: Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, Washington 98109, USA
Roland K. Strong: Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, Washington 98109, USA
Veronika Groh: Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, Washington 98109, USA
Thomas Spies: Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, Washington 98109, USA

Nature, 2007, vol. 447, issue 7143, 482-486

Abstract: Evasive tumours A number of advanced tumours appear to evade immune recognition by natural killer cells by shedding the soluble major histocompatibility complex class I-related ligand MICA, which inactivates the NKG2D receptor. New work in tumour cell cultures shows that the mechanism of this shedding process involves ERp5, a protein isomerase associated with the endoplasmic reticulum. This identifies surface ERp5 as a strategic target for therapeutic intervention to block tumour immune evasion.

Date: 2007
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DOI: 10.1038/nature05768

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