Journal
ONCOIMMUNOLOGY
Volume 7, Issue 2, Pages -Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/2162402X.2017.1385690
Keywords
antibody; checkpoint receptor; ligand; Tim-3; HDxMS
Categories
Funding
- National Institutes of Health [P01AI073748, R01NS045937, R01CA187975, R01DK51362]
- Melanoma Research Alliance
- Novartis
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI073748] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK051362, P30DK034854] Funding Source: NIH RePORTER
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Both in vivo data in preclinical cancer models and in vitro data with T cells from patients with advanced cancer support a role for Tim-3 blockade in promoting effective anti-tumor immunity. Consequently, there is considerable interest in the clinical development of antibody-based therapeutics that target Tim-3 for cancer immunotherapy. A challenge to this clinical development is the fact that several ligands for Tim-3 have been identified: galectin-9, phosphatidylserine, HMGB1, and most recently, CEACAM1. These observations raise the important question of which of these multiple receptor:ligand relationships must be blocked by an anti-Tim-3 antibody in order to achieve therapeutic efficacy. Here, we have examined the properties of anti-murine and anti-human Tim-3 antibodies that have shown functional efficacy and find that all antibodies bind to Tim-3 in a manner that interferes with Tim-3 binding to both phosphatidylserine and CEACAM1. Our data have implications for the understanding of Tim-3 biology and for the screening of anti-Tim-3 antibody candidates that will have functional properties in vivo.
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