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231225s2018 xx |||||o 00| ||eng c |
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7 |
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|a 10.1016/j.clim.2018.09.007
|2 doi
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|a pubmed24n0962.xml
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|a (DE-627)NLM288733258
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|a (NLM)30236770
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|a (PII)S1521-6616(18)30360-7
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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 Zhao, Chunmei
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a NLRP3 inflammasome regulates Th17 differentiation in rheumatoid arthritis
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| 264 |
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1 |
|c 2018
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| 336 |
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|a Text
|b txt
|2 rdacontent
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| 337 |
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 07.10.2019
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|a Date Revised 07.10.2019
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2018 Elsevier Inc. All rights reserved.
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|a Rheumatoid arthritis (RA) is one of the most common autoimmune diseases. Th17 has been shown to play am important role in the pathogenesis of RA. Accumulating data suggest the involvement of NLRP3 inflammasome in Th17 differentiation in autoimmune diseases. In the current study, we found that NLRP3 inflammasome is activated in CD4 T cells from RA patients. The activation of NLRP3 inflammasome was correlated with disease activities and IL-17A concentration in RA sera. Knockdown of NLRP3 suppressed Th17 differentiation. In addition, caspase-1 or IL-1 receptor inhibitor inhibits Th17 differentiation significantly. Further, ROS production is increased in CD4 T cells from RA patients. The inhibition of ROS production decreased NLRP3 inflammasome activation and IL-1β production in CD4 T cells, leading to the suppression of Th17 differentiation. These findings suggest a pathogenic role of NLRP3 inflammasome in RA by promoting Th17 cell differentiation. NLRP3 inflammasome could be a potential therapeutic target for the treatment of RA
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4 |
|a Journal Article
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|a Research Support, Non-U.S. Gov't
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| 650 |
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4 |
|a NLRP3 inflammasome
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| 650 |
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4 |
|a ROS
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| 650 |
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4 |
|a Rheumatoid arthritis
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| 650 |
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4 |
|a Th17 cells
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| 650 |
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7 |
|a Antioxidants
|2 NLM
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| 650 |
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|a Antirheumatic Agents
|2 NLM
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| 650 |
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|a Caspase Inhibitors
|2 NLM
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| 650 |
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|a IL1B protein, human
|2 NLM
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| 650 |
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|a Inflammasomes
|2 NLM
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| 650 |
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|a Interleukin 1 Receptor Antagonist Protein
|2 NLM
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| 650 |
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|a Interleukin-1beta
|2 NLM
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| 650 |
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7 |
|a MitoTEMPO
|2 NLM
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| 650 |
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7 |
|a NLR Family, Pyrin Domain-Containing 3 Protein
|2 NLM
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| 650 |
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|a NLRP3 protein, human
|2 NLM
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| 650 |
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|a Organophosphorus Compounds
|2 NLM
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| 650 |
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7 |
|a Piperidines
|2 NLM
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| 650 |
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|a Reactive Oxygen Species
|2 NLM
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| 650 |
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7 |
|a Receptors, Interleukin-1
|2 NLM
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| 650 |
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7 |
|a Caspase 1
|2 NLM
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| 650 |
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7 |
|a EC 3.4.22.36
|2 NLM
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| 700 |
1 |
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|a Gu, Yibin
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zeng, Xiaoyun
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Jing
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 197(2018) vom: 15. Dez., Seite 154-160
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:197
|g year:2018
|g day:15
|g month:12
|g pages:154-160
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| 856 |
4 |
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|u http://dx.doi.org/10.1016/j.clim.2018.09.007
|3 Volltext
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|a AR
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|d 197
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