Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/7745
Título
Disruption of the CCL1-CCR8 axis inhibits vascular Treg recruitment and function and promotes atherosclerosis in mice
Autor(es)
Vila-Caballer, Marian | Gonzalez-Granado, Jose Maria CNIC | Zorita, Virginia CNIC | Abu Nabah, Yafa N | Silvestre-Roig, Carlos CNIC | del Monte, Alberto CNIC | Molina-Sanchez, Pedro CNIC | Ait-Oufella, Hafid | Andres-Manzano, Maria J. CNIC | Sanz, María J | Weber, Christian | Kremer, Leonor | Gutiérrez, Julio | Mallat, Ziad | Andres, Vicente CNIC
Fecha de publicación
2019-07
Cita
J Mol Cell Cardiol. 2019; 132:154-163
Idioma
Inglés
Tipo de documento
journal article
Resumen
The CC chemokine 1 (CCL1, also called I-309 or TCA3) is a potent chemoattractant for leukocytes that plays an important role in inflammatory processes and diseases through binding to its receptor CCR8. Here, we investigated the role of the CCL1-CCR8 axis in atherosclerosis. We found increased expression of CCL1 in the aortas of atherosclerosis-prone fat-fed apolipoprotein E (Apoe)-null mice; moreover, in vitro flow chamber assays and in vivo intravital microscopy demonstrated an essential role for CCL1 in leukocyte recruitment. Mice doubly deficient for CCL1 and Apoe exhibited enhanced atherosclerosis in aorta, which was associated with reduced plasma levels of the anti-inflammatory interleukin 10, an increased splenocyte Th1/Th2 ratio, and a reduced regulatory T cell (Treg) content in aorta and spleen. Reduced Treg recruitment and aggravated atherosclerosis were also detected in the aortas of fat-fed low-density lipoprotein receptor-null mice treated with CCR8 blocking antibodies. These findings demonstrate that disruption of the CCL1-CCR8 axis promotes atherosclerosis by inhibiting interleukin 10 production and Treg recruitment and function.
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