2024-03-29T07:47:10Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1262522021-12-27T16:18:31Zcom_10261_79com_10261_1col_10261_332
DIGITAL.CSIC
author
Fuente, Hortensia de la
author
Bonay, Pedro
author
Sánchez-Madrid, Francisco
funder
Fundación Pro CNIC
funder
Ministerio de Ciencia e Innovación (España)
funder
Generalitat de Catalunya
funder
Ministerio de Economía y Competitividad (España)
funder
Instituto de Salud Carlos III
funder
Comunidad de Madrid
2015-12-01T09:23:12Z
2015-12-01T09:23:12Z
2014-04-21
Molecular and Cellular Biology 34: 2479- 2487 (2014)
http://hdl.handle.net/10261/126252
10.1128/MCB.00348-14
http://dx.doi.org/10.13039/501100004837http://dx.doi.org/10.13039/501100002809http://dx.doi.org/10.13039/501100003329http://dx.doi.org/10.13039/100012818http://dx.doi.org/10.13039/501100004587
24752896
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. © 2014, American Society for Microbiology.
eng
openAccess
The leukocyte activation receptor CD69 controls T cell differentiation through its interaction with galectin-1
artículo
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SánchezMadrid_TheLeukocyteActivationReceptor.pdf.txt