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231224s2011 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2011.08.003
|2 doi
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|a pubmed24n0705.xml
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|a (DE-627)NLM211470341
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|a (NLM)21917526
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Issekutz, Andrew C
|e verfasserin
|4 aut
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| 245 |
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|a Intravenous immunoglobulin G (IVIG) inhibits IL-1- and TNF-α-dependent, but not chemotactic-factor-stimulated, neutrophil transendothelial migration
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|c 2011
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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 20.12.2011
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|a Date Revised 10.12.2019
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2011 Elsevier Inc. All rights reserved.
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|a High-dose intravenous immunoglobulin (IVIG) has anti-inflammatory effects via incompletely understood mechanisms. By investigating whether IVIG might modulate neutrophil (PMN) recruitment, we observed that IVIG dose-dependently inhibited (by 30-50%) PMN transendothelial migration (TEM) across human umbilical vein endothelial cells (EC) stimulated with IL-1α, IL-1β, TNF-α or IL-1β+TNF-α. Inhibition required the presence of IVIG with the responding PMNs, was attributable to the F(ab)(2) portion and was unrelated to putative contaminants in IVIG. IVIG did not inhibit IL-1β- or TNF-α-induced increase of PMN adhesion to EC, nor did it affect C5a- or IL-8-induced PMN TEM across unstimulated EC. Effects of IVIG and F(ab)(2) fragments were not associated with PMN activation, assessed by CD62L shedding, CD11b upregulation or PMN shape. Thus, IVIG selectively inhibits PMN TEM across inflammatory-cytokine-stimulated - but not unstimulated - EC, perhaps contributing to therapeutic benefit in chronic inflammation with minimal impact on chemotactic-factor-induced PMN recruitment during acute infection
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|a Comparative Study
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|a Journal Article
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| 650 |
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|a Research Support, Non-U.S. Gov't
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| 650 |
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|a CD11b Antigen
|2 NLM
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| 650 |
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|a Chemotactic Factors
|2 NLM
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| 650 |
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|a ITGAM protein, human
|2 NLM
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| 650 |
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|a Immunoglobulin Fab Fragments
|2 NLM
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| 650 |
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|a Immunoglobulins, Intravenous
|2 NLM
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| 650 |
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|a Interleukin-1alpha
|2 NLM
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| 650 |
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7 |
|a Interleukin-1beta
|2 NLM
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| 650 |
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|a Interleukin-8
|2 NLM
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| 650 |
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|a Tumor Necrosis Factor-alpha
|2 NLM
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| 650 |
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|a L-Selectin
|2 NLM
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| 650 |
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|a 126880-86-2
|2 NLM
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| 650 |
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|a Complement C5a
|2 NLM
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| 650 |
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|a 80295-54-1
|2 NLM
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| 700 |
1 |
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|a Rowter, Derek
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Macmillan, Heather F
|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 141(2011), 2 vom: 15. Nov., Seite 187-96
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
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|g volume:141
|g year:2011
|g number:2
|g day:15
|g month:11
|g pages:187-96
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|u http://dx.doi.org/10.1016/j.clim.2011.08.003
|3 Volltext
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