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Mol Cell Biol. 2014 Jul;34(13):2479-87. doi: 10.1128/MCB.00348-14. Epub 2014 Apr 21.

The leukocyte activation receptor CD69 controls T cell differentiation through its interaction with galectin-1.

Author information

  • 1Servicio de Inmunología, Hospital de la Princesa, Universidad Autónoma de Madrid, Instituto Investigación Sanitaria Princesa, Madrid, Spain Department of Vascular Biology and Inflammation, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.
  • 2Servicio de Inmunología, Hospital de la Princesa, Universidad Autónoma de Madrid, Instituto Investigación Sanitaria Princesa, Madrid, Spain.
  • 3Department of Vascular Biology and Inflammation, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.
  • 4Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Cantoblanco, Madrid, Spain.
  • 5Laboratory of Cardiovascular Proteomics, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.
  • 6Cancer Research Program, Hospital del Mar Research Institute, Barcelona, Spain.
  • 7Neuroscience Research Program, Hospital del Mar Research Institute, and Pompeu Fabra University, Barcelona, Spain.
  • 8Servicio de Inmunología, Hospital de la Princesa, Universidad Autónoma de Madrid, Instituto Investigación Sanitaria Princesa, Madrid, Spain Department of Vascular Biology and Inflammation, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain fsanchez.hlpr@salud.madrid.org.

Abstract

CD69 is involved in immune cell homeostasis, regulating the T cell-mediated immune response through the control of Th17 cell differentiation. However, natural ligands for CD69 have not yet been described. Using recombinant fusion proteins containing the extracellular domain of CD69, we have detected the presence of a ligand(s) for CD69 on human dendritic cells (DCs). Pulldown followed by mass spectrometry analyses of CD69-binding moieties on DCs identified galectin-1 as a CD69 counterreceptor. Surface plasmon resonance and anti-CD69 blocking analyses demonstrated a direct and specific interaction between CD69 and galectin-1 that was carbohydrate dependent. Functional assays with both human and mouse T cells demonstrated the role of CD69 in the negative effect of galectin-1 on Th17 differentiation. Our findings identify CD69 and galectin-1 to be a novel regulatory receptor-ligand pair that modulates Th17 effector cell differentiation and function.

Copyright © 2014, American Society for Microbiology. All Rights Reserved.

PMID:
24752896
[PubMed - indexed for MEDLINE]
PMCID:
PMC4054309
Free PMC Article
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