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231224s2015 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2015.03.025
|2 doi
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|a pubmed25n0825.xml
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|a (DE-627)NLM247792896
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|a (NLM)25847223
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|a (PII)S1521-6616(15)00128-X
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Ortiz, M A
|e verfasserin
|4 aut
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|a IL-6 blockade reverses the abnormal STAT activation of peripheral blood leukocytes from rheumatoid arthritis patients
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|c 2015
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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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|a Date Completed 25.08.2015
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|a Date Revised 25.11.2016
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2015 Elsevier Inc. All rights reserved.
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|a Considering the interplay of multiple STATs in response to cytokines, we investigated how IL-6 and its blocking affect STAT signaling in rheumatoid arthritis (RA). Leukocytes obtained from RA patients before and after tocilizumab treatment and healthy donors (HDs) were cytokine-stimulated and STAT phosphorylation was analyzed by cytometry. RA patients had significantly fewer pSTAT1+, pSTAT3+, and pSTAT6+ monocytes and pSTAT5+ lymphocytes than HDs. After 24weeks of treatment, percentages of IFNγ-induced pSTAT1+ and IL-10-induced pSTAT3+ monocytes in RA patients increased, reaching levels comparable to HDs. pSTAT1+ and pSTAT3+ cells correlated inversely with RA disease activity index and levels of pSTAT+ cells at baseline were higher in patients with good EULAR response to tocilizumab. IFNγ-induced pSTAT1+ cells correlated inversely with memory T cells and anti-CCP levels. IL-10-induced pSTAT3+ cells correlated with Treg/Teff ratio. Our findings suggest that IL-6 blocking reduces the inflammatory mechanisms through the correction of STAT1 and STAT3 activation status
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a IL-6
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|a Leukocytes
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|a Rheumatoid arthritis
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|a STATs
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|a Tocilizumab
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|a Antibodies, Monoclonal, Humanized
|2 NLM
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|a Interleukin-6
|2 NLM
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|a Peptides, Cyclic
|2 NLM
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|a STAT1 Transcription Factor
|2 NLM
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|a STAT1 protein, human
|2 NLM
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|a STAT3 Transcription Factor
|2 NLM
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|a STAT3 protein, human
|2 NLM
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|a cyclic citrullinated peptide
|2 NLM
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|a tocilizumab
|2 NLM
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|a I031V2H011
|2 NLM
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1 |
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|a Diaz-Torné, C
|e verfasserin
|4 aut
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|a Hernández, M V
|e verfasserin
|4 aut
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|a Reina, D
|e verfasserin
|4 aut
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|a de la Fuente, D
|e verfasserin
|4 aut
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|a Castellví, I
|e verfasserin
|4 aut
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|a Moya, P
|e verfasserin
|4 aut
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|a Ruiz, J M
|e verfasserin
|4 aut
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|a Corominas, H
|e verfasserin
|4 aut
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|a Zamora, C
|e verfasserin
|4 aut
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|a Cantó, E
|e verfasserin
|4 aut
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|a Sanmartí, R
|e verfasserin
|4 aut
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|a Juarez, C
|e verfasserin
|4 aut
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|a Vidal, S
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 158(2015), 2 vom: 18. Juni, Seite 174-82
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:158
|g year:2015
|g number:2
|g day:18
|g month:06
|g pages:174-82
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|u http://dx.doi.org/10.1016/j.clim.2015.03.025
|3 Volltext
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|a AR
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|d 158
|j 2015
|e 2
|b 18
|c 06
|h 174-82
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