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Forum on Immunopathological Diseases and Therapeutics
SJR: 0.309 SNIP: 0.041 CiteScore™: 0.18

ISSN Imprimir: 2151-8017
ISSN En Línea: 2151-8025

Archives: Volume 1, 2010 to Volume 7, 2016

Forum on Immunopathological Diseases and Therapeutics

DOI: 10.1615/ForumImmunDisTher.v1.i4.50
pages 307-315

Toll-like Receptor 2 and 4 in Cancer Immunotherapy: Is Nitric Oxide a Mediator?

Amandine Martin
EPHE, Cancer Immunotherapy Laboratory, University of Burgundy, Dijon
Cedric Seignez
EPHE, Cancer Immunotherapy Laboratory, University of Burgundy, Dijon
Catherine Paul
EPHE, Cancer Immunotherapy Laboratory, University of Burgundy, Dijon
Ali Bettaieb
École Pratique des Hautes Études (EPHE), PSL Research University, Paris, France; Laboratoire d'Immunologie et Immunothérapie des Cancers (LIIC), Université de Bourgogne Franche-Comté, Dijon, France
Jean-Francois Jeannin
EPHE Tumor Immunology and Immunotherapy, Laboratory, University of Burgundy, Dijon, France


The main function of the immune system is to recognize and eliminate pathogens. Recognition of these organisms is done by binding of evolutionary conserved molecules called pathogen-associated molecular patterns (PAMPs) to specific receptors called pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), which are mainly expressed by immune cells. Tumor cells, which do not produce PAMPs, are therefore able to escape from immune surveillance. Consequently, effective cancer immunotherapies using PRR ligands were developed. Thus, the use of Bacillus Calmette-Guerin (BCG), a TLR-2 ligand, and Taxol, a TLR-4 ligand, have become standard cancer immunotherapies. In our laboratory, we have developed an efficient immunotherapy approach in murine models of colon and breast cancers with a lipid A analog, OM-174. After TLR-4 binding, OM-174 induces immune cell recruitment, inflammatory response activation, cytokine secretion, inducible nitric oxide synthase (iNOS) expression, and nitric oxide (NO) production in tumors. Moreover, although NO is not toxic itself for tumor cells, it could sensitize them to the death-induced by tumor necrosis factor (TNF)-family ligands such as the Fas ligand (FasL), TNF-related apoptosis-inducing ligand (TRAIL), and TNF-α. Thus, NO may play a mediator role in efficient immunotherapies based on TLR-2 and TLR-4 activation.

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