The leukocyte activation receptor CD69 controls T cell differentiation through its interaction with galectin-1
Entity
UAM. Departamento de MedicinaPublisher
American Society for MicrobiologyDate
2014-01-01Citation
10.1128/MCB.00348-14
Molecular and Cellular Biology 34.13 (2014): 2479–2487
ISSN
0270-7306 (print); 1098-5549 (online)DOI
10.1128/MCB.00348-14Funded by
This work was funded by grants SAF2011-25834 and ERC-2011AdG 294340-GENTRIS to F.S.-M., RECAVA RD06/0014 from the Fondo de Investigaciones Sanitarias to J.V. and F.S.-M., and INDISNET 01592006 from the Comunidad de Madrid to F.S.-M. and P.M. and by grants from the Ministerio de Economia y Competitividad (PI11/01562 to P.N.) and the Generalitat de Catalunya-AGAUR (2009SGR1409 to P.N.). The Ministry of Science and Innovation and the Pro-CNIC Foundation support CNICProject
Comunidad de Madrid. S2010/BMD-2332/INDISNETEditor's Version
http://dx.doi.org/:10.1128/MCB.00348-14Subjects
CD69; Cells; Interaction with Galectin-1; MedicinaRights
© 2014, American Society for MicrobiologyAbstract
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
Files in this item
Google Scholar:Fuente, Hortensia de la
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Cruz-Adalia, Aranzazu
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Martínez del Hoyo, Gloria
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Cibrián-Vera, Danay
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Bonay Miarons, Pedro
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Pérez-Hernández, Daniel
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Vázquez, Jesús
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Navarro, Pilar
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Gutierrez-Gallego, Ricardo
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Ramirez-Huesca, Marta
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Martín, Pilar
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Sánchez Madrid, Francisco
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