Linked Life Data

16293707

Source:http://linkedlifedata.com/resource/pubmed/id/16293707

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-1-5
pubmed:abstractText
The particular microenvironment of the skeletal muscle can be the site of complex immune reactions. Toll-like receptors (TLRs) mediate inflammatory stimuli from pathogens and endogenous danger signals and link the innate and adaptive immune system. We investigated innate immune responses in human muscle. Analyzing TLR1-9 mRNA in cultured myoblasts and rhabdomyosarcoma cells, we found constitutive expression of TLR3. The TLR3 ligand Poly (I:C), a synthetic analog of dsRNA, and IFN-gamma increased TLR3 levels. TLR3 was mainly localized intracellularly and regulated at the protein level. Poly (I:C) challenge 1) activated nuclear factor-kappaB (NF-kappaB), 2) increased IL-8 release, and 3) up-regulated NKG2D ligands and NK-cell-mediated lysis of muscle cells. We examined muscle biopsy specimens of 6 HIV patients with inclusion body myositis/polymyositis (IBM/PM), 7 cases of sporadic IBM and 9 nonmyopathic controls for TLR3 expression. TLR3 mRNA levels were elevated in biopsy specimens from patients with IBM and HIV-myopathies. Muscle fibers in inflammatory myopathies expressed TLR3 in close proximity of infiltrating mononuclear cells. Taken together, our study suggests an important role of TLR3 in the immunobiology of muscle, and has substantial implications for the understanding of the pathogenesis of inflammatory myopathies or therapeutic interventions like vaccinations or gene transfer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
118-20
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16293707-Cell Line, pubmed-meshheading:16293707-Gene Expression Regulation, pubmed-meshheading:16293707-HIV Infections, pubmed-meshheading:16293707-Humans, pubmed-meshheading:16293707-Inflammation, pubmed-meshheading:16293707-Interferon-gamma, pubmed-meshheading:16293707-Interleukin-8, pubmed-meshheading:16293707-Ligands, pubmed-meshheading:16293707-Muscle, Skeletal, pubmed-meshheading:16293707-Muscular Diseases, pubmed-meshheading:16293707-NF-kappa B, pubmed-meshheading:16293707-NK Cell Lectin-Like Receptor Subfamily K, pubmed-meshheading:16293707-RNA, Messenger, pubmed-meshheading:16293707-Receptors, Immunologic, pubmed-meshheading:16293707-Receptors, Natural Killer Cell, pubmed-meshheading:16293707-Signal Transduction, pubmed-meshheading:16293707-Toll-Like Receptor 3
pubmed:year
2006
pubmed:articleTitle
Expression of toll-like receptors by human muscle cells in vitro and in vivo: TLR3 is highly expressed in inflammatory and HIV myopathies, mediates IL-8 release and up-regulation of NKG2D-ligands.
pubmed:affiliation
Department of General Neurology, Hertie-Institute for Clinical Brain Research, Eberhard-Karls-University Tuebingen, Tuebingen, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't