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231224s2013 xx |||||o 00| ||eng c |
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7 |
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|a 10.1016/j.clim.2013.04.008
|2 doi
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| 028 |
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2 |
|a pubmed24n0759.xml
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|a (DE-627)NLM227712021
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|a (NLM)23697917
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|a (PII)S1521-6616(13)00108-3
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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 Moll, Monika
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a Inflammasome and cytokine blocking strategies in autoinflammatory disorders
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| 264 |
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1 |
|c 2013
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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 20.08.2013
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|a Date Revised 16.11.2017
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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| 520 |
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|a Copyright © 2013 Elsevier Inc. All rights reserved.
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|a Autoinflammatory disorders are characterized by usually unprovoked recurrent episodes of features of inflammation caused by activation of the innate immune system. Many autoinflammatory disorders - the monogenetic defects in particular - are associated with alterations of inflammasomes. Inflammasomes are complex multimolecular structures, which respond to "danger" signals by activation of cytokines. Among these, IL-1 is the key player of the innate immune response and inflammation. Consequently, IL-1 blocking strategies are specific pathway targeting therapies in autoinflammatory diseases and applied in CAPS, colchicine-resistant FMF, TRAPS, HIDS and DIRA. A number of rare genetic disorders involve inflammasome malfunction resulting in enhanced inflammatory response. IL-1 inhibition to date is the most successful specific therapy in autoinflammatory disorders. Here, current treatment strategies in autoinflammatory disorders are reviewed with a focus on inflammasome and cytokine inhibition
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| 650 |
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4 |
|a Journal Article
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| 650 |
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4 |
|a Research Support, Non-U.S. Gov't
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| 650 |
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4 |
|a Review
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| 650 |
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7 |
|a Antibodies, Monoclonal
|2 NLM
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| 650 |
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7 |
|a Antibodies, Monoclonal, Humanized
|2 NLM
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| 650 |
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7 |
|a Antirheumatic Agents
|2 NLM
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| 650 |
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7 |
|a Inflammasomes
|2 NLM
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| 650 |
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7 |
|a Interleukin 1 Receptor Antagonist Protein
|2 NLM
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| 650 |
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7 |
|a Interleukin-1
|2 NLM
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| 650 |
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7 |
|a NF-kappa B p50 Subunit
|2 NLM
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| 650 |
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7 |
|a NFKB1 protein, human
|2 NLM
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| 650 |
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7 |
|a Recombinant Fusion Proteins
|2 NLM
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| 650 |
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7 |
|a canakinumab
|2 NLM
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| 650 |
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7 |
|a 37CQ2C7X93
|2 NLM
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| 650 |
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7 |
|a rilonacept
|2 NLM
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| 650 |
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7 |
|a 8K80YB5GMG
|2 NLM
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| 650 |
|
7 |
|a gevokizumab
|2 NLM
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| 650 |
|
7 |
|a QX3JU54GYQ
|2 NLM
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| 700 |
1 |
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|a Kuemmerle-Deschner, Jasmin B
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 147(2013), 3 vom: 03. Juni, Seite 242-75
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:147
|g year:2013
|g number:3
|g day:03
|g month:06
|g pages:242-75
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| 856 |
4 |
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|u http://dx.doi.org/10.1016/j.clim.2013.04.008
|3 Volltext
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|d 147
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