Toll-like receptor 9-dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE (Q29620722)

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Bierhaus A

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author name string

Tian J

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Avalos AM

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Mao SY

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Chen B

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Senthil K

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Wu H

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Parroche P

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Drabic S

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Golenbock D

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Sirois C

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Hua J

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An LL

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Audoly L

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La Rosa G

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Naworth P

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Marshak-Rothstein A

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Crow MK

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Fitzgerald KA

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Latz E

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Kiener PA

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Coyle AJ

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publication date

May 2007

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volume

8

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issue

5

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page(s)

487-96

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Pathogenesis of systemic lupus erythematosus

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Measurement of increases in anti-double-stranded DNA antibody levels as a predictor of disease exacerbation in systemic lupus erythematosus. A long-term, prospective study

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Necessity of oligonucleotide aggregation for toll-like receptor 9 activation

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Nucleic acids of mammalian origin can act as endogenous ligands for Toll-like receptors and may promote systemic lupus erythematosus

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Properties regulating the nature of the plasmacytoid dendritic cell response to Toll-like receptor 9 activation

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Intracellular localization of Toll-like receptor 9 prevents recognition of self DNA but facilitates access to viral DNA.

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Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

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HMG-1 as a late mediator of endotoxin lethality in mice

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Role of HMGB1 in apoptosis-mediated sepsis lethality

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HMGB1 is a potent trigger of arthritis

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Reversing established sepsis with antagonists of endogenous high-mobility group box 1.

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High mobility group box chromosomal protein 1: A novel proinflammatory mediator in synovitis

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RAGE is the major receptor for the proinflammatory activity of HMGB1 in rodent macrophages

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High mobility group box 1 protein interacts with multiple Toll-like receptors

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The receptor for advanced glycation end products (RAGE) is a cellular binding site for amphoterin. Mediation of neurite outgrowth and co-expression of rage and amphoterin in the developing nervous system

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Requirement of HMGB1 and RAGE for the maturation of human plasmacytoid dendritic cells

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Release of high mobility group box 1 by dendritic cells controls T cell activation via the receptor for advanced glycation end products

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Increased expression of the novel proinflammatory cytokine high mobility group box chromosomal protein 1 in skin lesions of patients with lupus erythematosus

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On spectral relaxation in proteins.

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Activation of autoreactive B cells by CpG dsDNA

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Functional assay of type I interferon in systemic lupus erythematosus plasma and association with anti-RNA binding protein autoantibodies

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Induction of interferon-alpha production in plasmacytoid dendritic cells by immune complexes containing nucleic acid released by necrotic or late apoptotic cells and lupus IgG.

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TLR9/MyD88 signaling is required for class switching to pathogenic IgG2a and 2b autoantibodies in SLE.

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Immunology. Discriminating microbe from self suffers a double toll

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Toll-like receptor activation in the pathogenesis of systemic lupus erythematosus

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New EMBO members' review: the double life of HMGB1 chromatin protein: architectural factor and extracellular signal

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Selected Toll-like receptor agonist combinations synergistically trigger a T helper type 1-polarizing program in dendritic cells

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Recombinant HMGB1 with cytokine-stimulating activity

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High mobility group 1 protein (HMG-1) stimulates proinflammatory cytokine synthesis in human monocytes

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The high mobility group (HMG) boxes of the nuclear protein HMG1 induce chemotaxis and cytoskeleton reorganization in rat smooth muscle cells

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Extracellular HMGB1, a signal of tissue damage, induces mesoangioblast migration and proliferation

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Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells

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HMGB1 B box increases the permeability of Caco-2 enterocytic monolayers and impairs intestinal barrier function in mice

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Amphoterin stimulates myogenesis and counteracts the antimyogenic factors basic fibroblast growth factor and S100B via RAGE binding

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Antagonism of RAGE suppresses peripheral nerve regeneration

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Blockade of RAGE–amphoterin signalling suppresses tumour growth and metastases

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High mobility group B1 protein suppresses the human plasmacytoid dendritic cell response to TLR9 agonists.

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Monocytic cells hyperacetylate chromatin protein HMGB1 to redirect it towards secretion

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Chromatin-IgG complexes activate B cells by dual engagement of IgM and Toll-like receptors

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Bacterial CpG-DNA and lipopolysaccharides activate Toll-like receptors at distinct cellular compartments

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The receptor for advanced glycation end-products (RAGE) directly binds to ERK by a D-domain-like docking site

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Activation of the interferon-alpha pathway identifies a subgroup of systemic lupus erythematosus patients with distinct serologic features and active disease.

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Identifiers

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30 April 2017

Consolidated OpenCitations Corpus – April 2017

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Consolidated OpenCitations Corpus – April 2017

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PubMed publication ID

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30 April 2017

Consolidated OpenCitations Corpus – April 2017