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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| Autores principales: | , |
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| Formato: | CHAP |
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| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_97814899_v_n_p347_Dimitroff |
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| Sumario: | 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. |
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