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(Circulation Research. 2004;95:e96.)
© 2004 American Heart Association, Inc.

Letter to the Editor

Role of Toll-Like Receptors in Atherosclerosis

Kathrin S. Michelsen

Division of Infectious Diseases and Immunology and, The Atherosclerosis Research Center, Burns and Allen Research Institute, Cedars-Sinai Medical Center and, David Geffen School of Medicine at UCLA, Los Angeles, Calif

Terence M. Doherty

Division of Cardiology and, The Atherosclerosis Research Center, Burns and Allen Research Institute, Cedars-Sinai Medical Center and, David Geffen School of Medicine at UCLA, Los Angeles, Calif

Prediman K. Shah

Division of Cardiology and, The Atherosclerosis Research Center, Burns and Allen Research Institute, Cedars-Sinai Medical Center and, David Geffen School of Medicine at UCLA, Los Angeles, Calif

Moshe Arditi

Division of Infectious Diseases and Immunology and, The Atherosclerosis Research Center, Burns and Allen Research Institute, Cedars-Sinai Medical Center and, David Geffen School of Medicine at UCLA, Los Angeles, Calif, moshe.arditi@cshs.org

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read with interest both the recent paper by Dunzendorfer et al¹ and the accompanying commentary.² We wish to clarify some key points. Dunzendorfer et al report that under antiatherogenic conditions of laminar flow, human coronary artery endothelial cells (ECs) express low levels of Toll-like receptor 2 (TLR2) mRNA and protein. Dunzendorfer et al also reported that TLR2 mRNA and protein expression was increased under conditions of low shear stress and that laminar flow resulted in protein kinase CK2 phosphorylation of SP1, which inhibited binding of SP1 to the TLR2 promoter. These results conflict in part with data published 2 years previously by Liang et al,³ although the authors did not cite this work. That study showed low levels of TLR2 mRNA expression in ECs under laminar flow. There was no change in TLR2 expression but increased TLR4 expression and nuclear factor B activation with low shear stress in ECs.

Moreover, the totality of data reported to date do not unequivocally demonstrate TLR2 expression by ECs that is functionally relevant and, instead, support a much more prominent role for TLR4-mediated signaling in ECs in diseases such as atherosclerosis. It is conceivable that coronary artery ECs, which are exposed to somewhat different hemodynamic forces from microvessel or venous ECs, might express a different repertoire of TLRs. However, human aortic ECs are exposed to similar hemodynamic stresses as coronary artery ECs, and Walton et al were unable to detect transcripts encoding TLR2 in these cells.⁴ Furthermore, in our hands, . . . [Full Text of this Article]

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