Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity

Galectin-1 (Gal-1), a member of an ancient family of animal glycan-binding proteins, has been implicated in a variety of biological events. Interactions between Gal-1 and Gal-1 ligands on T cells are critically involved in regulating the nature and intensity of T-cell-mediated inflammation and antit...

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Detalles Bibliográficos
Publicado: 2014
Materias:
Adaptive immunity
Galectin-1
Galectin-1 ligands
Galectin-1 therapeutics
Galectins
Inflammation
Tumor immunology
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_97814899_v_n_p347_Dimitroff
http://hdl.handle.net/20.500.12110/paper_97814899_v_n_p347_Dimitroff
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
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spelling paper:paper_97814899_v_n_p347_Dimitroff2023-06-08T16:37:50Z Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity Adaptive immunity Galectin-1 Galectin-1 ligands Galectin-1 therapeutics Galectins Inflammation Tumor immunology Galectin-1 (Gal-1), a member of an ancient family of animal glycan-binding proteins, has been implicated in a variety of biological events. Interactions between Gal-1 and Gal-1 ligands on T cells are critically involved in regulating the nature and intensity of T-cell-mediated inflammation and antitumor immunity. Appropriately glycosylated T-cell-membrane glycoconjugates operationally defined as Gal-1 ligands bind Gal-1 and elicit downstream cellular activities that dampen effector T-cell function. Together, these biological constituents represent promising targets in the development of novel anti-inflammatory and antitumor immune therapies. Whether through characteristic elevations in tumor-derived Gal-1 or an imbalance in regulatory and Gal-1 ligand+ effector T-cell subsets during inflammation, the Gal-1-Gal-1 ligand-binding axis offers numerous cellular/tissue contexts to strategically interfere with Gal-1 efficacy. In this chapter, we will examine recent assessments of (1) Gal-1 expression and function in controlling both adaptive and antitumor T-cell immunity, (2) identity and function of T-cell Gal-1 ligands, and (3) targeting of the Gal-1-Gal-1 ligand axis to regulate inflammation or boost antitumor immune responses. These research disciplines collectively highlight the importance of understanding the identity and functional nature of Gal-1 and its ligands to strategically and safely manipulate the immune system to control immunopathologic conditions. © Springer Science+Business Media, LLC 2014. All rights are reserved. 2014 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_97814899_v_n_p347_Dimitroff http://hdl.handle.net/20.500.12110/paper_97814899_v_n_p347_Dimitroff
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Adaptive immunity
Galectin-1
Galectin-1 ligands
Galectin-1 therapeutics
Galectins
Inflammation
Tumor immunology
spellingShingle Adaptive immunity
Galectin-1
Galectin-1 ligands
Galectin-1 therapeutics
Galectins
Inflammation
Tumor immunology
Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity
topic_facet Adaptive immunity
Galectin-1
Galectin-1 ligands
Galectin-1 therapeutics
Galectins
Inflammation
Tumor immunology
description Galectin-1 (Gal-1), a member of an ancient family of animal glycan-binding proteins, has been implicated in a variety of biological events. Interactions between Gal-1 and Gal-1 ligands on T cells are critically involved in regulating the nature and intensity of T-cell-mediated inflammation and antitumor immunity. Appropriately glycosylated T-cell-membrane glycoconjugates operationally defined as Gal-1 ligands bind Gal-1 and elicit downstream cellular activities that dampen effector T-cell function. Together, these biological constituents represent promising targets in the development of novel anti-inflammatory and antitumor immune therapies. Whether through characteristic elevations in tumor-derived Gal-1 or an imbalance in regulatory and Gal-1 ligand+ effector T-cell subsets during inflammation, the Gal-1-Gal-1 ligand-binding axis offers numerous cellular/tissue contexts to strategically interfere with Gal-1 efficacy. In this chapter, we will examine recent assessments of (1) Gal-1 expression and function in controlling both adaptive and antitumor T-cell immunity, (2) identity and function of T-cell Gal-1 ligands, and (3) targeting of the Gal-1-Gal-1 ligand axis to regulate inflammation or boost antitumor immune responses. These research disciplines collectively highlight the importance of understanding the identity and functional nature of Gal-1 and its ligands to strategically and safely manipulate the immune system to control immunopathologic conditions. © Springer Science+Business Media, LLC 2014. All rights are reserved.
title Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity
title_short Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity
title_full Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity
title_fullStr Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity
title_full_unstemmed Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity
title_sort defining the fate and function of effector t cells through galectin-1-galectin-1 ligand-binding interactions: implications in tumor immunity
publishDate 2014
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_97814899_v_n_p347_Dimitroff
http://hdl.handle.net/20.500.12110/paper_97814899_v_n_p347_Dimitroff
_version_ 1768541822730108928

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