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231225s2019 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2019.05.012
|2 doi
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|a pubmed24n1224.xml
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|a (NLM)31121287
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|a (PII)S1521-6616(19)30209-8
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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1 |
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|a Luo, Qin
|e verfasserin
|4 aut
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|a Interleukin 28 is a potential therapeutic target for sepsis
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|c 2019
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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
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|2 rdacarrier
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|a Date Completed 20.04.2020
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|a Date Revised 13.12.2023
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2019 Elsevier Inc. All rights reserved.
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|a Identification of new therapeutic targets for the treatment of sepsis is imperative. We report here that cytokine IL-28 (IFN-λ) levels were elevated in clinical and experimental sepsis. Neutralization of IL-28 protected mice from lethal sepsis induced by cecal ligation and puncture (CLP), which was associated with improved bacterial clearance and enhanced neutrophil infiltration. Conversely, administration of recombinant IL-28 aggravated mortality, facilitated bacterial dissimilation and limited neutrophil recruitment, in the model of sepsis induced by CLP. This study defines IL-28 as a detrimental mediator during sepsis and identifies a potential therapeutic target for the immune therapy in sepsis
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Immunity
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|a Infection
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|a Interleukin-28
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|a Neutrophil
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|a Sepsis
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|a Antibodies, Neutralizing
|2 NLM
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|a Cytokines
|2 NLM
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|a interferon-lambda, human
|2 NLM
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|a IL28A protein, mouse
|2 NLM
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|a Interleukins
|2 NLM
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|a interferon-lambda protein, mouse
|2 NLM
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700 |
1 |
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|a Liu, Yi
|e verfasserin
|4 aut
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1 |
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|a Liu, Shuang
|e verfasserin
|4 aut
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1 |
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|a Yin, Yibing
|e verfasserin
|4 aut
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1 |
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|a Xu, Banglao
|e verfasserin
|4 aut
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700 |
1 |
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|a Cao, Ju
|e verfasserin
|4 aut
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0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 205(2019) vom: 22. Aug., Seite 29-34
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:205
|g year:2019
|g day:22
|g month:08
|g pages:29-34
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|u http://dx.doi.org/10.1016/j.clim.2019.05.012
|3 Volltext
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