2026-06-26T10:00:21Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/77452024-09-27T08:40:33Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Vila-Caballer, Marian author Gonzalez-Granado, Jose Maria author Zorita, Virginia author Abu Nabah, Yafa N author Silvestre-Roig, Carlos author del Monte, Alberto author Molina-Sanchez, Pedro author Ait-Oufella, Hafid author Andres-Manzano, Maria J. author Sanz, María J author Weber, Christian author Kremer, Leonor author Gutiérrez, Julio author Mallat, Ziad author Andres, Vicente author 2019-07 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. J Mol Cell Cardiol. 2019; 132:154-163 10.1016/j.yjmcc.2019.05.009 1095-8584 0022-2828 Journal of molecular and cellular cardiology 31121182 http://hdl.handle.net/20.500.12105/7745 Atherosclerosis CCL1 CCR8 IL-10 Treg Disruption of the CCL1-CCR8 axis inhibits vascular Treg recruitment and function and promotes atherosclerosis in mice