The Leukocyte Activation Receptor CD69 Controls T Cell Differentiation through Its Interaction with Galectin-1
The Leukocyte Activation Receptor CD69 Controls T Cell Differentiation through Its Interaction with Galectin-1
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DOI：
10.1128/mcb.00348-14
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发表时间：
2014-07-01
影响因子：
5.3
通讯作者：
Sanchez-Madrid, Francisco
中科院分区：
文献类型：
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作者：
de la Fuente, Hortensia;Cruz-Adalia, Aranzazu;Sanchez-Madrid, Francisco
CD 69参与免疫细胞稳态，通过控制Th 17细胞分化来调节T细胞介导的免疫应答。然而，CD 69的天然配体尚未被描述。使用含有CD 69胞外结构域的重组融合蛋白，我们已经检测到人树突状细胞（DC）上CD 69的配体的存在。下拉，然后质谱分析的CD 69结合部分的DC鉴定半乳糖凝集素-1作为CD 69的反受体。表面等离子体共振和抗CD 69阻断分析表明，CD 69和半乳糖凝集素-1之间的直接和特异性相互作用是碳水化合物依赖性的。人和小鼠T细胞的功能测定证明了CD 69在半乳糖凝集素-1对Th 17分化的负面影响中的作用。我们的研究结果确定CD 69和galectin-1是一种新的调节受体-配体对，调节Th 17效应细胞的分化和功能。
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). Pull-down 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.