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Citations to this article

Modulation of atherosclerosis in mice by Toll-like receptor 2
Adam E. Mullick, … , Peter S. Tobias, Linda K. Curtiss
Adam E. Mullick, … , Peter S. Tobias, Linda K. Curtiss
Published November 1, 2005
Citation Information: J Clin Invest. 2005;115(11):3149-3156. https://doi.org/10.1172/JCI25482.
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Modulation of atherosclerosis in mice by Toll-like receptor 2

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Abstract

Epidemiologic evidence has established a relationship between microbial infection and atherosclerosis. Mammalian TLRs provide clues on the mechanism of this inflammatory cascade. TLR2 has a large ligand repertoire that includes bacterial-derived exogenous and possibly host-derived endogenous ligands. In atherosclerosis-susceptible low-density lipoprotein receptor–deficient (Ldlr–/–) mice, complete deficiency of TLR2 led to a reduction in atherosclerosis. However, with BM transplantation, loss of TLR2 expression from BM-derived cells had no effect on disease progression. This suggested that an unknown endogenous TLR2 agonist influenced lesion progression by activating TLR2 in cells that were not of BM cell origin. Moreover, with intraperitoneal administration of a synthetic TLR2/TLR1 agonist, Pam3CSK4, disease burden was dramatically increased in Ldlr–/– mice. A complete deficiency of TLR2 in Ldlr–/– mice, as well as a deficiency of TLR2 only in BM-derived cells in Ldlr–/– mice, led to striking protection against Pam3CSK4-mediated atherosclerosis, suggesting a role for BM-derived cell expression of TLR2 in transducing the effects of an exogenous TLR2 agonist. These studies support the concept that chronic or recurrent microbial infections may contribute to atherosclerotic disease. Additionally, these data suggest the presence of host-derived endogenous TLR2 agonists.

Authors

Adam E. Mullick, Peter S. Tobias, Linda K. Curtiss

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Total citations by year

Year: 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 Total
Citations: 7 6 9 7 14 12 8 12 6 13 11 16 20 30 19 17 20 7 1 235
Citation information
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