SOD3 boosts T cell infiltration by normalizing the tumor endothelium and inducing laminin-α4

descriptionPublicationkeyboard_double_arrow_right Article 01 Jan 2020 Spain English Publisher:Informa UK LimitedJournal:OncoImmunology, volume 9 (eissn: 2162-402X,

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Authors: Carmona-Rodríguez, Lorena; Martínez Rey, Diego; Mira, Emilia; Mañes, Santos;

doi: 10.1080/2162402x.2020.1794163

pmid: 32934887

pmc: PMC7466848

handle: 10261/218385

SOD3 boosts T cell infiltration by normalizing the tumor endothelium and inducing laminin-α4

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Abstract

The conversion of a non-T cell-inflamed into a T cell-inflamed tumor microenvironment (TME) is a key to sensitizing tumors to T-cell-based immunotherapies. Recent data show that the extracellular superoxide dismutase (SOD3) alters endothelial basement membrane (EC-BM) composition, providing permissive signals that enhance tumor infiltration by effector T cells.AJ, adherens junction; EC, endothelial cell; EC-BM, endothelial basement membrane; HIF, hypoxia-inducible factor; ICAM-1, intercellular adhesion molecule-1; LAMA4, laminin-α4; SOD3, superoxide dismutase-3; TME, tumor microenvironment; VCAM-1, vascular cell adhesion molecule-1; VEGF, vascular-endothelial growth factor.

Country

Spain

Related Organizations

Spanish National Research Council
Spain
National Center for Biotechnology
Spain

Keywords

tumor, endothelium, extracellular matrix, T-Lymphocytes, til, laminin, Neoplasms, Tumor Microenvironment, oxidative stress, Humans, Author's View, RC254-282, adoptive cell transfer, Superoxide Dismutase, diapedesis, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, TIL, Extracellular matrix, RC581-607, Normalization, normalization, Oxidative stress, immunotherapy, Endothelium, Vascular, Laminin, Immunologic diseases. Allergy

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