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Article citations


Tsan, M. and Gao, B. (2004) Endogenous ligands of Tolllike receptors. Journal of Leukocyte Biology, 76, 514-519. doi:10.1189/jlb.0304127

has been cited by the following article:

  • TITLE: Association of monoctye expression of Toll-like receptor 4 and its related cytokines with coronary luminal stenosis

    AUTHORS: Bahador Bagheri, Bahram Sohrabi, Aliakbar Movassaghpur, Simin Mashayekhi, Afagh Garjani, Mehriar Shokri, Mohammad Noori, Alireza Garjani

    KEYWORDS: Atherosclerosis; Cytokines; Inflammation; hTLR4

    JOURNAL NAME: Advances in Bioscience and Biotechnology, Vol.4 No.7A, July 16, 2013

    ABSTRACT: Toll-like receptors are well-defined barriers in innate immunity. Among them hTLR4 on the surface of monocytes, plays a critical role in the formation of atherosclerotic plaques, plaque instability and arterial remodeling through production of inflammatory cytokines. This study was designed to examine the association of hTLR4 monocyte expression and response with the severity of coronary stenosis in patients with stable angina (SA). Blood samples were obtained from 39 patients with SA who were scheduled for a coronary angiography and from 28 healthy volunteers. The samples were collected before the procedure. Expression of hTLR4 on CD14+ monocytes and serum levels of TNF-α and IL-1β were measured using flowcytometry and ELISA techniques respectively. Percentage stenosis diameter was measured by comparing the area of coronary stenosis to an adjacent normal segment of the vessel. Compared with control group, patients showed upregulation of hTLR4+/CD14+ monocytes. Furthermore, patients with more severe coronary stenosis exhibited enhanced expression of hTLR4+/CD14+ monocytes (p α (p β. In addition, significant correlations were seen between percentage stenosis diameter and monocyte expression of hTLR4 as well as TNF-α. hTLR4 monocytic expression and related cytokines are positively associated percentage stenosis diameter. These results suggest that hTLR4 activity may be involved in progression of atherosclerosis.