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Inflamed by TLR4 internalization [PDF]
Immunology The pattern recognition receptor Toll-like receptor 4 (TLR4) stimulates the production of proinflammatory cytokines when activated on the cell surface, but endocytosed TLR4 signals through different effectors to drive the production of an antiviral cytokine called interferon-β. Metwally et al.
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TLR4 polymorphisms and disease susceptibility
Inflammation Research, 2012Toll-like receptors (TLRs) play a central role in the regulation of the host immune system. Each TLR recognizes specific pathogen-associated molecular patterns (PAMPs). TLR4 is one of the well characterized pathogen recognition receptors (PRRs) that recognizes the lipopolysaccharide (LPS) of Gram-negative bacteria, some conserved structures from fungal
Sheeba Murad Mall +7 more
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Science Signaling, 2013 
Cytoplasmic lipopolysaccharide from Gram-negative bacteria can activate the innate immune system directly.
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Cytoplasmic lipopolysaccharide from Gram-negative bacteria can activate the innate immune system directly.
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Regulators of TLR4 Signaling by Endotoxins
2010The stimulation of TLR4 by LPS activates two distinct signaling pathways leading to the expression of diverse inflammatory genes. Intensive studies over the past decade have revealed the components involved in these signaling pathways, however, more recently the focus has shifted somewhat towards the components that regulate these pathways.
Luke A. J. O'Neill, Anne F. McGettrick
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TLR4 in Toxoplasmosis; friends or foe?
Microbial Pathogenesis, 2014Toxoplasma species are obligate intracellular protozoan which are responsible for induction of several forms of Toxoplasmosis in humans. The mechanisms responsible for the progression of the prolonged forms of Toxoplasmosis and associated pathologies are yet to be identified.
Mohammad Zare-Bidaki +5 more
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TLR4 and LPS hyporesponsiveness in humans
International Journal of Hygiene and Environmental Health, 2002Asthma is a complex genetic disorder that is caused by a number of unique gene-gene and gene-environment interactions. The search for asthma susceptibility genes has been complicated by the broad clinical phenotype of asthma, the polygenic inheritance pattern of this disease, and the substantial role of environmental exposures in the development and ...
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2020 
Intracellular part of TLR4 signaling starts on the inner side of the cytoplasm and consists of two branches, namely, TLR4/TRIF/IRF3 and TLR4/MyD88/NF-κB. Through complex interactions including phosphorylation and ubiquitination, they lead to the activation of various transcription factors and are intrinsically regulated.
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Intracellular part of TLR4 signaling starts on the inner side of the cytoplasm and consists of two branches, namely, TLR4/TRIF/IRF3 and TLR4/MyD88/NF-κB. Through complex interactions including phosphorylation and ubiquitination, they lead to the activation of various transcription factors and are intrinsically regulated.
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Trends in Microbiology, 2002 
The recognition of microbial pathogens based on their molecular patterns is essential for host defense. Recently, Toll-like receptors have been shown not only to recognize viruses as well as bacteria and fungi, but also to trigger an efficient immune response.
Hans Acha-Orbea +3 more
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The recognition of microbial pathogens based on their molecular patterns is essential for host defense. Recently, Toll-like receptors have been shown not only to recognize viruses as well as bacteria and fungi, but also to trigger an efficient immune response.
Hans Acha-Orbea +3 more
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Science Signaling, 2009 
Activation of TLR4 by the extracellular matrix glycoprotein tenascin-C promotes persistent inflammation in mouse models of rheumatoid arthritis.
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Activation of TLR4 by the extracellular matrix glycoprotein tenascin-C promotes persistent inflammation in mouse models of rheumatoid arthritis.
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Cigarette Smoke Upregulates TLR4 Expression and Enhances TLR4 Mediated Responses
2006A key component of the innate defence mecbanisms against infections is represented by the tolllike receptor (TLR) family. We explored the role played by TLR4 in the pathogenesis of chronic obstructive pulmonary disease (COPD). We first assessed TLR4 expression by immunohystochemistry in surgical specimens from current and former smoker COPDs, from ...
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