Limits...
Toll-like receptor 4 in atherosclerosis.

Li H, Sun B - J. Cell. Mol. Med. (2007 Jan-Feb)

Bottom Line: Toll-like receptor 4 (TLR4) is key regulators of both innate and adaptive immune responses.TLR4 recognizes pathogen-associated molecular patterns (PAMPs) and activates the inflammatory cells.These studies have shown that TLR4 function affects the initiation and progression of atherosclerosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Shanghai Jiaotong University Affiliated First People's Hospital, 85 Wujin Road, Shanghai 200080, PR China.

ABSTRACT
Toll-like receptor 4 (TLR4) is key regulators of both innate and adaptive immune responses. TLR4 recognizes pathogen-associated molecular patterns (PAMPs) and activates the inflammatory cells. The function of TLR4 in atherosclerosis has been investigated in mouse knockout studies and epidemiological studies of human TLR4 polymorphisms. These studies have shown that TLR4 function affects the initiation and progression of atherosclerosis. This article reviews the biological functions and clinical implications of TLR4 in atherosclerosis.

Show MeSH

Related in: MedlinePlus

TLR4 signaling pathway and its relation with atherosclerosis. Both endogenous and exogenous ligands can activate TLR4 on cells, such as endothelial cells, vascular smooth muscle cells, adventitial fibroblasts, dendritic cells and macrophages. Activated TLR4 lead to activation of the transcription factor nuclear factor κ B-(NF-κB) or IRF3-responsive genes. Activated transcription factors mediate secretion of pro-inflammatory cytokines and chemokines and also induce expression of adhesion molecules. Ultimately, these processes might initiate or promote atherosclerotic lesions.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4401222&req=5

fig01: TLR4 signaling pathway and its relation with atherosclerosis. Both endogenous and exogenous ligands can activate TLR4 on cells, such as endothelial cells, vascular smooth muscle cells, adventitial fibroblasts, dendritic cells and macrophages. Activated TLR4 lead to activation of the transcription factor nuclear factor κ B-(NF-κB) or IRF3-responsive genes. Activated transcription factors mediate secretion of pro-inflammatory cytokines and chemokines and also induce expression of adhesion molecules. Ultimately, these processes might initiate or promote atherosclerotic lesions.

Mentions: Activation of TLR4 was shown to elicit the production of cytokines and chemokines [15]. Therefore, it was suggested that the TLR4 might be involved in immune responses, especially in the activation of innate immunity. Activated TLR4 triggers not only innate immunity but also adaptive immunity. TLR4 activation on dendritic cells induces the expression of co-stimulatory molecules and production of inflammatory cytokines [16]. Then, activated dendritic cells present microorganism-derived peptide antigens expressed on the cell surface with MHC class II antigen to naive T cells, thereby initiating an antigen-specific adaptive immune response [17]. Now, evidence is accumulating that TLR4 could affect atherosclerosis in multiple ways (Fig. 1).


Toll-like receptor 4 in atherosclerosis.

Li H, Sun B - J. Cell. Mol. Med. (2007 Jan-Feb)

TLR4 signaling pathway and its relation with atherosclerosis. Both endogenous and exogenous ligands can activate TLR4 on cells, such as endothelial cells, vascular smooth muscle cells, adventitial fibroblasts, dendritic cells and macrophages. Activated TLR4 lead to activation of the transcription factor nuclear factor κ B-(NF-κB) or IRF3-responsive genes. Activated transcription factors mediate secretion of pro-inflammatory cytokines and chemokines and also induce expression of adhesion molecules. Ultimately, these processes might initiate or promote atherosclerotic lesions.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4401222&req=5

fig01: TLR4 signaling pathway and its relation with atherosclerosis. Both endogenous and exogenous ligands can activate TLR4 on cells, such as endothelial cells, vascular smooth muscle cells, adventitial fibroblasts, dendritic cells and macrophages. Activated TLR4 lead to activation of the transcription factor nuclear factor κ B-(NF-κB) or IRF3-responsive genes. Activated transcription factors mediate secretion of pro-inflammatory cytokines and chemokines and also induce expression of adhesion molecules. Ultimately, these processes might initiate or promote atherosclerotic lesions.
Mentions: Activation of TLR4 was shown to elicit the production of cytokines and chemokines [15]. Therefore, it was suggested that the TLR4 might be involved in immune responses, especially in the activation of innate immunity. Activated TLR4 triggers not only innate immunity but also adaptive immunity. TLR4 activation on dendritic cells induces the expression of co-stimulatory molecules and production of inflammatory cytokines [16]. Then, activated dendritic cells present microorganism-derived peptide antigens expressed on the cell surface with MHC class II antigen to naive T cells, thereby initiating an antigen-specific adaptive immune response [17]. Now, evidence is accumulating that TLR4 could affect atherosclerosis in multiple ways (Fig. 1).

Bottom Line: Toll-like receptor 4 (TLR4) is key regulators of both innate and adaptive immune responses.TLR4 recognizes pathogen-associated molecular patterns (PAMPs) and activates the inflammatory cells.These studies have shown that TLR4 function affects the initiation and progression of atherosclerosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Shanghai Jiaotong University Affiliated First People's Hospital, 85 Wujin Road, Shanghai 200080, PR China.

ABSTRACT
Toll-like receptor 4 (TLR4) is key regulators of both innate and adaptive immune responses. TLR4 recognizes pathogen-associated molecular patterns (PAMPs) and activates the inflammatory cells. The function of TLR4 in atherosclerosis has been investigated in mouse knockout studies and epidemiological studies of human TLR4 polymorphisms. These studies have shown that TLR4 function affects the initiation and progression of atherosclerosis. This article reviews the biological functions and clinical implications of TLR4 in atherosclerosis.

Show MeSH
Related in: MedlinePlus