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20231224201830.0 |
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231224s2016 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2016.07.010
|2 doi
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|a pubmed24n0874.xml
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|a (DE-627)NLM262478277
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|a (NLM)27422491
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|a (PII)S1521-6616(16)30185-1
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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 Tojima, Ichiro
|e verfasserin
|4 aut
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|a Group 2 innate lymphoid cells are increased in nasal polyps in patients with eosinophilic chronic rhinosinusitis
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|c 2016
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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 30.03.2017
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|a Date Revised 30.03.2022
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2016 Elsevier Inc. All rights reserved.
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|a ILC2s represent a critical innate cellular source of type 2 cytokines and may play important roles in various diseases. We examined the role of ILC2s in the pathogenesis of two subgroups of CRSwNP: ECRS and non-ECRS. We analyzed the prevalence of ILC2s in sinonasal tissues and in blood from patients with ECRS, non-ECRS, CRSsNP, and control. The prevalence of ILC2s in nasal tissues was higher in patients with ECRS as compared to those with non-ECRS or CRSsNP. The prevalence of blood ILC2s was not different between patients with ECRS and non-ECRS. The prevalence of blood ILC2s was higher in patients with allergic rhinitis and elevated serum IgE levels. Alternaria-induced IL-33 secretion was increased in nasal epithelial cells derived from patients with ECRS as compared to those from patients with non-ECRS or CRSsNP. ILC2s may be involved in the pathogenesis of CRSwNP, in particular in patients with tissue eosinophilia (i.e., ECRS)
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Allergic rhinitis
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|a Alternaria
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|a Asthma
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|a Eosinophilic chronic rhinosinusitis
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|a Group 2 innate lymphoid cells
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|a IL-33
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|a Cytokines
|2 NLM
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|a Interleukin-33
|2 NLM
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1 |
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|a Kouzaki, Hideaki
|e verfasserin
|4 aut
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1 |
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|a Shimizu, Shino
|e verfasserin
|4 aut
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1 |
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|a Ogawa, Takao
|e verfasserin
|4 aut
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1 |
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|a Arikata, Masahiko
|e verfasserin
|4 aut
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1 |
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|a Kita, Hirohito
|e verfasserin
|4 aut
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700 |
1 |
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|a Shimizu, Takeshi
|e verfasserin
|4 aut
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773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 170(2016) vom: 15. Sept., Seite 1-8
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:170
|g year:2016
|g day:15
|g month:09
|g pages:1-8
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|u http://dx.doi.org/10.1016/j.clim.2016.07.010
|3 Volltext
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