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231224s2012 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2012.07.012
|2 doi
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|a pubmed24n0735.xml
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|a (DE-627)NLM220677239
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|a (NLM)22940633
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|a (PII)S1521-6616(12)00187-8
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Hofmann, Sigrun R
|e verfasserin
|4 aut
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| 245 |
1 |
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|a Attenuated TLR4/MAPK signaling in monocytes from patients with CRMO results in impaired IL-10 expression
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|c 2012
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| 336 |
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 27.11.2012
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|a Date Revised 11.03.2022
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2012 Elsevier Inc. All rights reserved.
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|a Chronic recurrent multifocal osteomyelitis (CRMO) is an autoinflammatory bone disorder of unknown origin. We previously demonstrated that monocytes from CRMO patients fail to express the immune-modulatory cytokine interleukin-10 (IL-10) in a chromatin dependent manner. Here, we demonstrate that attenuated extracellular-signal regulated kinase (ERK)1 and 2 signaling in response to TLR4 activation results in failure to induce IL-10 expression in monocytes from CRMO patients. Attenuated ERK1/2 activation results in 1) reduced levels of Sp-1, a transcription factor that induces IL-10 expression in monocytes, and 2) impaired H3S10 phosphorylation of the IL10 promoter, an activating epigenetic mark. The pro-inflammatory cytokines tumor necrosis factor (TNF)α and IL-6 are not negatively affected, resulting in an imbalance towards pro-inflammatory cytokines. Thus, impaired ERK1/2 signaling with subsequently reduced Sp-1 expression and H3S10 phosphorylation of the IL10 promoter may centrally contribute to the pathophysiology of CRMO
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Chromatin
|2 NLM
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|a IL10 protein, human
|2 NLM
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|a Interleukin-6
|2 NLM
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|a TLR4 protein, human
|2 NLM
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| 650 |
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|a Toll-Like Receptor 4
|2 NLM
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| 650 |
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|a Tumor Necrosis Factor-alpha
|2 NLM
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| 650 |
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|a Interleukin-10
|2 NLM
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| 650 |
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|a 130068-27-8
|2 NLM
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| 650 |
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|a Protein Kinases
|2 NLM
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| 650 |
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|a EC 2.7.-
|2 NLM
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| 650 |
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|a Sp1 kinase
|2 NLM
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| 650 |
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|a EC 2.7.1.-
|2 NLM
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| 650 |
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|a MAPK1 protein, human
|2 NLM
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| 650 |
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|a EC 2.7.11.24
|2 NLM
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| 650 |
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|a Mitogen-Activated Protein Kinase 1
|2 NLM
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| 650 |
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7 |
|a EC 2.7.11.24
|2 NLM
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| 650 |
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|a Mitogen-Activated Protein Kinase 3
|2 NLM
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| 650 |
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|a EC 2.7.11.24
|2 NLM
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| 700 |
1 |
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|a Morbach, Henner
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Schwarz, Tobias
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Rösen-Wolff, Angela
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Girschick, Hermann J
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Hedrich, Christian M
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 145(2012), 1 vom: 15. Okt., Seite 69-76
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
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|g volume:145
|g year:2012
|g number:1
|g day:15
|g month:10
|g pages:69-76
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| 856 |
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|u http://dx.doi.org/10.1016/j.clim.2012.07.012
|3 Volltext
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|d 145
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|h 69-76
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