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

Hortensia de la Fuente, Aranzazu Cruz-Adalia, Gloria Martinez del Hoyo, Danay Cibrián-Vera, Pedro Bonay, Daniel Pérez-Hernández, Jesús Vázquez, Pilar Navarro, Ricardo Gutierrez-Gallego, Marta Ramirez-Huesca, Pilar Martín, Francisco Sánchez-Madrid*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

53 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)2479-2487
Number of pages9
JournalMolecular and Cellular Biology
Volume34
Issue number13
DOIs
Publication statusPublished - Jul 2014
Externally publishedYes

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