Toll To Be Paid at the Gateway to the Vessel Wall

Hansson, Göran K.; Edfeldt, Kristina

doi:10.1161/01.atv.0000168894.43759.47

Cited by 86 publications

(45 citation statements)

References 32 publications

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“…The mammalian analog, the Toll-like receptor, was first cloned in 1997 (578), and by now at least 11 human and 13 mouse TLRs have been described (519,676). Toll-like receptors are coupled to a complex signaling pathways (which, for most of TLRs except TRL3 involves adaptor protein MyD88) that end at the transcription factor AP-1 and/or in the nuclear translocation of another transcription factor NF-B (355,426).…”

Section: A Toll-like Receptorsmentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,090

2,981

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Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed “resting microglia.” Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the “activated microglial cell.” This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.

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Section: A Toll-like Receptorsmentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,090

2,981

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“…6,8 -10 The role of TLR4 in vascular remodeling, especially arterial remodeling, has previously been demonstrated in various studies either directed at atherogenesis and plaque (de)stabilization or directed at the role of TLR4 in postinterventional arterial remodeling after angioplasty. [11][12][13][14][15][16] However, the role of TLR4 and its endogenous ligands in remodeling of venous segments (eg, in vein graft remodeling) is still unknown. Furthermore, it has been suggested that unactivated arterial vascular smooth muscle cells (VSMC) do not express TLR4 and that TLRs may have a vessel-specific profile that may also vary because of changes in cellular activation, differentiation, and other local processes.…”

mentioning

confidence: 99%

Toll-Like Receptor 4 Is Involved in Human and Mouse Vein Graft Remodeling, and Local Gene Silencing Reduces Vein Graft Disease in Hypercholesterolemic APOE*3Leiden Mice

Karper

Vries

Brand

et al. 2011

ATVB

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Objective-The goal of this study was to explore the role of Toll-like receptor 4 (TLR4) in vein graft remodeling and disease. Methods and Results-First, expression of TLR4 was analyzed in freshly isolated human saphenous veins (huSV), in freshly isolated huSV ex vivo perfused in an extracorporeal circulation, or in huSV used as coronary vein grafts. Marked induction of focal TLR4 expression was observed in perfused fresh huSV. Moreover, TLR4 was abundantly present in lesions in fresh huSV or in intimal hyperplasia in coronary vein grafts. Second, mouse venous bypass grafting was performed. In grafts of hypercholesterolemic APOE*3Leiden mice, increased TLR4 mRNA and protein was detected over time by reverse transcription-polymerase chain reaction and immunohistochemistry. Furthermore, the local presence of the endogenous TLR4 ligands heat shock protein 60, high-mobility group box 1, tenascin-C, and biglycan in the grafts was demonstrated. TLR4 deficiency in C3H-Tlr4 LPS-d (LPS indicates lipopolysaccharide) mice resulted in 48Ϯ12% less vein graft wall thickening (Pϭ0.04) than in Balb/c controls. Moreover, local TLR4 gene silencing in hypercholesterolemic APOE*3Leiden mice using lentiviral short hairpin RNA against TLR4 administered perivascularly around vein grafts led to a 44Ϯ13% reduction of vessel wall thickening compared with controls (Pϭ0.0059). Conclusion-These

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“…which translates as "That's great!" [26]. Jules Hoffmann, Bruce Beutler and Ralph Steinman (discoverer of DCs) won the Nobel Prize in 2011 for the discovery of TLRs in humans [27].…”

Section: Toll-like Receptors (Tlrs)mentioning

confidence: 99%

Immune Recognition in Lung Diseases: Basic Research and Clinical Application

Alvarado¹,

Arce²

2016

Clin Infect Immun

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Respiratory diseases are among the leading causes of morbidity and mortality in the world population. Our understanding of the molecular mechanisms leading to recognition of infectious pathogens and harmful endogenous signals by the innate immune system and the adaptive immune system has improved significantly in recent decades. There is increased evidence of the key role of the immune system with its pattern recognition receptors (PRRs) in infectious and non-infectious lung diseases. The PRRs are a family of sensors able to sense different microbial molecules as well as endogenous molecules which are released by the host tissue damage. The commitment of PRRs is a prerequisite for the initiation of immune and inflammatory response to infection and tissue injury that may be beneficial or harmful. The PRRs are germ-line encoded, evolutionarily conserved molecules and consist of Toll-like receptors, NOD-like receptors, RIG-I-like receptors, C-type lectin-like receptors and cytosolic DNA sensors. This review summarizes the prominent role of transmembrane and cytosolic PRRs in the pathogenesis of infectious and non-infectious lung diseases. The PRRs and their signals represent promising targets for prophylactic and therapeutic strategies in various lung diseases.

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Toll To Be Paid at the Gateway to the Vessel Wall

Cited by 86 publications

References 32 publications

Physiology of Microglia

Physiology of Microglia

Toll-Like Receptor 4 Is Involved in Human and Mouse Vein Graft Remodeling, and Local Gene Silencing Reduces Vein Graft Disease in Hypercholesterolemic APOE*3Leiden Mice

Immune Recognition in Lung Diseases: Basic Research and Clinical Application

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