Combined Inhibition of CCL2, CX3CR1, and CCR5 Abrogates Ly6C hi and Ly6C lo Monocytosis and Almost Abolishes Atherosclerosis in Hypercholesterolemic Mice
Author(s) -
Christophe Combadière,
Stéphane Potteaux,
Mathieu P. Rodero,
Tabassome Simon,
Adeline Pézard,
Bruno Esposito,
Régine Merval,
Amanda E. I. Proudfoot,
Alain Tedgui,
Ziad Mallat
Publication year - 2008
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.107.745091
Subject(s) - monocytosis , medicine , monocyte , cx3cr1 , ccr2 , chemokine , bone marrow , immunology , chemokine receptor , ccl2 , myeloid , macrophage , inflammation , biology , biochemistry , in vitro
Monocytes are critical mediators of atherogenesis. Deletion of individual chemokines or chemokine receptors leads to significant but only partial inhibition of lesion development, whereas deficiency in other signals such as CXCL16 or CCR1 accelerates atherosclerosis. Evidence that particular chemokine pathways may cooperate to promote monocyte accumulation into inflamed tissues, particularly atherosclerotic arteries, is still lacking.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom