Transcriptional Regulation of the Endogenous Danger Signal Tenascin-C: A Novel Autocrine Loop in Inflammation

Goh, Fui G.; Piccinini, Anna M.; Krausgruber, Thomas; Udalova, Irina A.; Midwood, Kim S.

doi:10.4049/jimmunol.0903359

Cited by 135 publications

(111 citation statements)

References 54 publications

(48 reference statements)

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“…The synthesis and tissue expression were induced in myeloid cells upon tissue injury or infection Thus, tenascin-C acted as TLR4 activator and novel autocrine loop in the arthritis. 147,148 S100A8 is a strong promoter of activating FcgRI and FcgRIV in macrophages through the activation of TLR4 and act as a regulator of FcgR expression in inflamed synovium in chronic experimental arthritis.…”

Section: Experimental Arthritis Induced By Pamps and Dampsmentioning

confidence: 99%

“…In RA synovial tissues and/or fluid, several DAMPs have been suggested to act as stimulators of TLRs ; biglycan, 12,13,163 fibrinogen, 164,165 fibronectin EDA (FENDA), 166,167 HMGB1, 168 HSP70, 169,170 HSP B8 (HSP22), 171 low molecular weigh hyarulonic acid, 172,173 S100A8/9 174-176 and tenascin-C. 148,[177][178][179] These molecules have potential to stimulate TLRs, thus evoke and/or enhance innate immune system, and couple with adoptive immune reaction in RA.…”

Section: Pamps and Damps In Ra Synovial Tissuesmentioning

confidence: 99%

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Toll-like Receptor

Takagi

2011

J Clin Exp Hematopathol

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Toll like receptor (TLR), one of the key functions of innate immune system, can recognize not only exogenous pathogenassociated molecular patterns, namely PAMPs, but also endogenous molecules created upon tissue injury, sterile inflammation and degeneration. Endogenous TLR ligands are called as damage-associated molecular patters (DAMPs), including endogenous molecules released by activated and necrotic cells, and extracellular matrix molecules. DAMPs are also known as alarmins. TLR research has brought about new insights in the rheumatic diseases. Previous reports suggest that TLRs and the signal pathways intensively contribute to the pathogenesis of rheumatoid arthritis (RA) and other arthritic conditions with interaction of various TLR ligands. Accumulated knowledge of TLR system is summarized to overlook TLRs and the signaling pathway in arthritis conditions, with special reference to RA. 〔J Clin Exp Hematopathol 51(2) : 77-92, 2011〕

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Section: Experimental Arthritis Induced By Pamps and Dampsmentioning

confidence: 99%

Section: Pamps and Damps In Ra Synovial Tissuesmentioning

confidence: 99%

Toll-like Receptor

Takagi

2011

J Clin Exp Hematopathol

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“…Another positive feedback loop may be the basis of chronic inflammation in arthritis, where inflammatory cytokines induce tenascin-C expression, which in turn activates TLR4 signaling in fibroblasts and myeloid cells leading to more cytokine production and more tenascin-C secretion. This establishes a vicious cycle causing chronic inflammation (Goh et al 2010;). …”

Section: Regulation Of Tenascin Expressionmentioning

confidence: 99%

Tenascins and the Importance of Adhesion Modulation

Chiquet‐Ehrismann¹,

Tucker²

2011

Cold Spring Harbor Perspectives in Biology

203

187

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“…41 On the other side, this pathway or others may increase TNC production by the dermal or immune cells, as inflammatory stimuli activate the PI3 kinase/AKT and NF-kB signaling pathway in myeloid cells. 42 Another avenue for exploration involves tracking changes in TNC levels with response or resistance to generalized or targeted therapies. Still, these molecular targets needs to be better defined to develop new therapeutic approaches.…”

Section: Regulation Of Tnc Expression In Melanomamentioning

confidence: 99%