Identification of CD112R as a novel checkpoint for human T cells

J Exp Med. 2016 Feb 8;213(2):167-76. doi: 10.1084/jem.20150785.

Yuwen Zhu ¹, Alessandro Paniccia ², Alexander C Schulick ², Wei Chen ³, Michelle R Koenig ², Joshua T Byers ², Sheng Yao ⁴, Shaun Bevers ⁵, Barish H Edil ¹

Affiliations

1 Department of Surgery, Anschutz Medical Campus, University of Colorado, Aurora, CO 80045 yuwen.zhu@ucdenver.edu barish.edil@ucdenver.edu.
2 Department of Surgery, Anschutz Medical Campus, University of Colorado, Aurora, CO 80045.
3 Department of Surgery, Anschutz Medical Campus, University of Colorado, Aurora, CO 80045 Department of Hepatobiliary and Pancreatic Surgery, Second Affiliated Hospital, Zhejiang University, 310027 Hangzhou, China.
4 TopAlliance Biosciences, Inc., Rockville, MD 20850.
5 Department of Biochemistry and Molecular Genetics, Anschutz Medical Campus, University of Colorado, Aurora, CO 80045.

PMID: 26755705 DOI: 10.1084/jem.20150785

Abstract

T cell immunoglobulin and ITIM domain (TIGIT) and CD226 emerge as a novel T cell cosignaling pathway in which CD226 and TIGIT serve as costimulatory and coinhibitory receptors, respectively, for the ligands CD155 and CD112. In this study, we describe CD112R, a member of poliovirus receptor-like proteins, as a new coinhibitory receptor for human T cells. CD112R is preferentially expressed on T cells and inhibits T cell receptor-mediated signals. We further identify that CD112, widely expressed on antigen-presenting cells and tumor cells, is the ligand for CD112R with high affinity. CD112R competes with CD226 to bind to CD112. Disrupting the CD112R-CD112 interaction enhances human T cell response. Our experiments identify CD112R as a novel checkpoint for human T cells via interaction with CD112.

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