Commentary 10.1172/JCI125471
1Department of Biomedical Engineering,
2Department of Pathology, Medicine and Oncology, and
3Immunology Program, Institute of Cellular Engineering, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Address correspondence to: Jonathan Schneck, Department of Pathology, Johns Hopkins University School of Medicine, 733 N. Broadway, Miller Research Building Room 639, Baltimore, Maryland 21205, USA. Phone: 410.614.4589; Email: jschnec1@jhmi.edu.
Find articles by Isser, A. in: JCI | PubMed | Google Scholar
1Department of Biomedical Engineering,
2Department of Pathology, Medicine and Oncology, and
3Immunology Program, Institute of Cellular Engineering, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Address correspondence to: Jonathan Schneck, Department of Pathology, Johns Hopkins University School of Medicine, 733 N. Broadway, Miller Research Building Room 639, Baltimore, Maryland 21205, USA. Phone: 410.614.4589; Email: jschnec1@jhmi.edu.
Find articles by Schneck, J. in: JCI | PubMed | Google Scholar
First published December 10, 2018 - More info
Adoptive cell transfer (ACT) of engineered T cell receptors (TCRs) for cancer immunotherapy has evolved from simple gene transfer of isolated TCRs to various affinity enhancement techniques that overcome limitations imposed by central and peripheral tolerance on TCR affinity. In the current issue of the JCI, Poncette et al. used mice with human TCRαβ and HLA gene loci to discover CD4+ TCRs of optimal affinity for cancer testis antigen (CTA) NY-ESO-1. They combined this TCR with a previously discovered NY-ESO-1–specific CD8+ TCR in an ACT fibrosarcoma tumor model to demonstrate the importance of T cell help in mediating antitumor responses.
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