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231224s2015 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2014.10.008
|2 doi
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|a pubmed24n0813.xml
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|a (DE-627)NLM244049165
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|a (NLM)25450336
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|a (PII)S1521-6616(14)00244-7
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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 Furukawa, Sachiko
|e verfasserin
|4 aut
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|a Preferential M2 macrophages contribute to fibrosis in IgG4-related dacryoadenitis and sialoadenitis, so-called Mikulicz's disease
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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 26.02.2015
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|a Date Revised 17.03.2022
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2014. Published by Elsevier Inc.
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|a IgG4-related dacryoadenitis and sialoadenitis (IgG4-DS) is characterized by bilateral swelling of glandular tissues with extensive fibrosis, and is immunologically considered a Th2-predominant disease. Recent studies reported that alternatively activated (M2) macrophages enhanced Th2 immune responses and fibrosis by production of pro-fibrotic factors (IL-10, IL-13 and CCL18). Therefore, we examined the association between M2 macrophages and fibrosis in submandibular glands from 7 patients with IgG4-DS, 10 patients with chronic sialoadenitis, 10 patients with Sjögren's syndrome, and 10 healthy subjects. The number of M2 macrophages in SMGs from patients with IgG4-DS was also significantly higher than in the other groups. Double immunofluorescence staining showed that IL-10 and CCL18 expression co-localized with M2 macrophage-marker (CD163). Furthermore, the SMG fibrosis score was positively correlated with the frequency of M2 macrophages in only IgG4-DS. These results indicate that IL-10 and CCL18 secreted by preferential M2 macrophages possibly play a key role in the development of severe fibrosis in IgG4-DS
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a CCL18
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|a Fibrosis;
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|a IL-10;
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|a IgG4-related dacryoadenitis and sialoadenitis;
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|a M2 macrophage;
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|a CCL18 protein, human
|2 NLM
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|a Chemokines, CC
|2 NLM
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|a Immunoglobulin G
|2 NLM
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|a Interleukin-10
|2 NLM
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|a 130068-27-8
|2 NLM
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1 |
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|a Moriyama, Masafumi
|e verfasserin
|4 aut
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1 |
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|a Tanaka, Akihiko
|e verfasserin
|4 aut
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700 |
1 |
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|a Maehara, Takashi
|e verfasserin
|4 aut
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700 |
1 |
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|a Tsuboi, Hiroto
|e verfasserin
|4 aut
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700 |
1 |
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|a Iizuka, Mana
|e verfasserin
|4 aut
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1 |
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|a Hayashida, Jun-Nosuke
|e verfasserin
|4 aut
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700 |
1 |
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|a Ohta, Miho
|e verfasserin
|4 aut
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1 |
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|a Saeki, Takako
|e verfasserin
|4 aut
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1 |
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|a Notohara, Kenji
|e verfasserin
|4 aut
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1 |
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|a Sumida, Takayuki
|e verfasserin
|4 aut
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700 |
1 |
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|a Nakamura, Seiji
|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 156(2015), 1 vom: 30. Jan., Seite 9-18
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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773 |
1 |
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|g volume:156
|g year:2015
|g number:1
|g day:30
|g month:01
|g pages:9-18
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|u http://dx.doi.org/10.1016/j.clim.2014.10.008
|3 Volltext
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|a GBV_USEFLAG_A
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|a GBV_ILN_11
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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|d 156
|j 2015
|e 1
|b 30
|c 01
|h 9-18
|