2. Academic Validation
  3. Modulation of CD6 function through interaction with Galectin-1 and -3

Modulation of CD6 function through interaction with Galectin-1 and -3

  • FEBS Lett. 2014 Aug 25;588(17):2805-13. doi: 10.1016/j.febslet.2014.05.064.
Cristina Escoda-Ferran 1,  Esther Carrasco 1,  Miguel Caballero-Baños 2,  Cristina Miró-Julià 1,  Mario Martínez-Florensa 1,  Marta Consuegra-Fernández 1,  Vanesa G Martínez 1,  Fu-Tong Liu 3,  Francisco Lozano 4
Affiliations

Affiliations

  • 1 From Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centre Esther Koplowitz, 08036 Barcelona, Spain.
  • 2 Servei d'Immunologia, Centre de Diagnòstic Biomèdic, Hospital Clínic de Barcelona, 08036 Barcelona, Spain.
  • 3 Department of Dermatology, UC Davis School of Medicine, Sacramento, CA 95816, United States.
  • 4 From Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centre Esther Koplowitz, 08036 Barcelona, Spain; Servei d'Immunologia, Centre de Diagnòstic Biomèdic, Hospital Clínic de Barcelona, 08036 Barcelona, Spain; Departament de Biologia Cel lular, Immunologia i Neurociències, Facultat de Medicina Universitat de Barcelona, 08036 Barcelona, Spain. Electronic address: [email protected].
PMID: 24945728 DOI: 10.1016/j.febslet.2014.05.064
Abstract

CD6 is a lymphocyte glycoprotein receptor that physically associates with the antigen-specific receptor complex at the center of the immunological synapse, where it interacts with its ligand CD166/ALCAM. The present work reports the carbohydrate-dependent interaction of CD6 and CD166/ALCAM with Galectin-1 and -3, two well-known soluble mammalian lectins. Both galectins interfered with superantigen-induced T cell proliferation and cell adhesion phenomena mediated by the CD6-CD166/ALCAM pair, while CD6 expression protected cells from galectin-induced Apoptosis. The results suggest that interaction of Galectin-1 and -3 with CD6 and CD166/ALCAM might modulate some relevant aspects of T cell physiology.

Keywords

ALCAM/CD166; Apoptosis; CD6; Cell adhesion; Galectin; T-cell activation.

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