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dc.creatorPalazon, A. (Asís)-
dc.creatorTeijeira, A. (Álvaro)-
dc.creatorMartinez-Forero, I. (Iván)-
dc.creatorHervas-Stubbs, S. (Sandra)-
dc.creatorRoncal, C. (Carmen)-
dc.creatorPeñuelas-Sanchez, I. (Ivan)-
dc.creatorDubrot, J. (Juan)-
dc.creatorMorales-Kastresana, A. (Aizea)-
dc.creatorPerez-Gracia, J.L. (Jose Luis)-
dc.creatorOchoa, M.C. (María Carmen)-
dc.creatorOchoa, L. (Laura)-
dc.creatorMartinez, A. (Alfredo)-
dc.creatorLuque, A. (Alfonso)-
dc.creatorDinchuk, J. (Joseph)-
dc.creatorRouzaut, A. (Ana)-
dc.creatorJure-Kunkel, M. (María)-
dc.creatorMelero, I. (Ignacio)-
dc.date.accessioned2011-12-20T14:54:45Z-
dc.date.available2011-12-20T14:54:45Z-
dc.date.issued2011-
dc.identifier.citationPalazon A, Teijeira A, Martinez-Forero I, Hervas-Stubbs S, Roncal C, Penuelas I, et al. Agonist anti-CD137 mAb act on tumor endothelial cells to enhance recruitment of activated T lymphocytes. Cancer Res 2011 Feb 1;71(3):801-811.es_ES
dc.identifier.issn1538-7445-
dc.identifier.urihttps://hdl.handle.net/10171/20317-
dc.description.abstractAgonist monoclonal antibodies (mAb) to the immune costimulatory molecule CD137, also known as 4-1BB, are presently in clinical trials for cancer treatment on the basis of their costimulatory effects on primed T cells and perhaps other cells of the immune system. Here we provide evidence that CD137 is selectively expressed on the surface of tumor endothelial cells. Hypoxia upregulated CD137 on murine endothelial cells. Treatment of tumor-bearing immunocompromised Rag(-/-) mice with agonist CD137 mAb did not elicit any measurable antiangiogenic effects. In contrast, agonist mAb stimulated tumor endothelial cells, increasing cell surface expression of the adhesion molecules intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, and E-selectin. When adoptively transferred into mice, activated T lymphocytes derived from CD137-deficient animals entered more avidly into tumor tissue after treatment with agonist mAb. This effect could be neutralized with anti-ICAM-1 and anti-VCAM-1 blocking antibodies. Thus, stimulation of CD137 not only enhanced T-cell activation but also augmented their trafficking into malignant tissue, through direct actions on the blood vessels that irrigate the tumor. Our findings identify an additional mechanism of action that can explain the immunotherapeutic effects of agonist CD137 antibodies.es_ES
dc.language.isoenges_ES
dc.publisherAmerican Association for Cancer Researches_ES
dc.rightsinfo:eu-repo/semantics/closedAccess-
dc.subjectAntibodies, Monoclonal/pharmacologyes_ES
dc.subjectAntigens, CD137/agonistses_ES
dc.subjectEndothelial Cells/drug effectses_ES
dc.subjectT-Lymphocytes/immunologyes_ES
dc.titleAgonist anti-CD137 mAb act on tumor endothelial cells to enhance recruitment of activated T lymphocyteses_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherversionhttp://cancerres.aacrjournals.org/content/71/3/801es_ES
dc.type.driverinfo:eu-repo/semantics/articlees_ES

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