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Abstract:

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.

Registro:

Documento: Parte de libro
Título:Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity
Autor:Dimitroff, C.J.; Rabinovich, G.A.
Filiación:Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, United States
Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, C1428ADN, Argentina
Palabras clave:Adaptive immunity; Galectin-1; Galectin-1 ligands; Galectin-1 therapeutics; Galectins; Inflammation; Tumor immunology
Año:2014
Página de inicio:347
Página de fin:367
DOI: http://dx.doi.org/10.1007/978-1-4899-8056-4_12
Título revista:Tumor-Induced Immune Suppression: Mechanisms and Therapeutic Reversal
Título revista abreviado:Tum.-Induc. Immune Suppr.: Mechanisms and Therapeut. Reversal
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_97814899_v_n_p347_Dimitroff

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Citas:

---------- APA ----------
Dimitroff, C.J. & Rabinovich, G.A. (2014) . Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity. Tumor-Induced Immune Suppression: Mechanisms and Therapeutic Reversal, 347-367.
http://dx.doi.org/10.1007/978-1-4899-8056-4_12
---------- CHICAGO ----------
Dimitroff, C.J., Rabinovich, G.A. "Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity" . Tumor-Induced Immune Suppression: Mechanisms and Therapeutic Reversal (2014) : 347-367.
http://dx.doi.org/10.1007/978-1-4899-8056-4_12
---------- MLA ----------
Dimitroff, C.J., Rabinovich, G.A. "Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity" . Tumor-Induced Immune Suppression: Mechanisms and Therapeutic Reversal, 2014, pp. 347-367.
http://dx.doi.org/10.1007/978-1-4899-8056-4_12
---------- VANCOUVER ----------
Dimitroff, C.J., Rabinovich, G.A. Defining the fate and function of effector T cells through galectin-1-galectin-1 ligand-binding interactions: Implications in tumor immunity. Tum.-Induc. Immune Suppr.: Mechanisms and Therapeut. Reversal. 2014:347-367.
http://dx.doi.org/10.1007/978-1-4899-8056-4_12