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231225s2018 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2018.05.007
|2 doi
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|a pubmed24n0951.xml
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|a (DE-627)NLM285507540
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|a (NLM)29906512
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|a (PII)S1521-6616(18)30195-5
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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 Zhang, Rui
|e verfasserin
|4 aut
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|a Mechanisms of fibronectin-binding protein A (FnBPA110-263) vaccine efficacy in Staphylococcus aureus sepsis versus skin infection
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|c 2018
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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 14.08.2019
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|a Date Revised 14.08.2019
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2018 Elsevier Inc. All rights reserved.
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|a Increasing rates of life-threatening infections and decreasing susceptibility to antibiotics urge an effective vaccine targeting Staphylococcus aureus. Here we investigate the role of cellular immunity in FnBPA110-263 mediated protection in Staphylococcus aureus infection. This study revealed FnBPA110-263 broadly protected mice from seven FnBPA isotypes strains in the sepsis model. FnBPA110-263 immunized B-cell deficient mice were protected against lethal challenge, while T-cell deficient mice were not. Reconstituting mice with FnBPA110-263 specific CD4+ T-cells conferred antigen specific protection. In vitro assays indicated that isolated FnBPA110-263 specific splenocytes from immunized mice produced abundant IL-17A. IL-17A deficient mice were not protected from a lethal challenge by FnBPA110-263 vaccination. Moreover, neutralizing IL-17A, but not IFN-γ,reverses FnBPA110-263-induced protective efficacy in sepsis and skin infection model. These findings suggest that IL-17A producing Th17 cells play an essential role in FnBPA110-263 vaccine-mediated defense against S. aureus sepsis and skin infection in mice
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Fibronectin-binding protein A
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|a Immune protection
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|a Staphylococcus aureus
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|a Th17
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|a Vaccine
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|a Adhesins, Bacterial
|2 NLM
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|a Bacterial Vaccines
|2 NLM
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|a Interleukin-17
|2 NLM
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|a fibronectin-binding proteins, bacterial
|2 NLM
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650 |
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|a Interferon-gamma
|2 NLM
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650 |
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|a 82115-62-6
|2 NLM
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700 |
1 |
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|a Li, Sun
|e verfasserin
|4 aut
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700 |
1 |
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|a Zhang, Xiao-Kai
|e verfasserin
|4 aut
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700 |
1 |
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|a Wang, Yu
|e verfasserin
|4 aut
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700 |
1 |
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|a Yang, Liu-Yang
|e verfasserin
|4 aut
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700 |
1 |
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|a Zeng, Hao
|e verfasserin
|4 aut
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700 |
1 |
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|a Yan, Da-Peng
|e verfasserin
|4 aut
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700 |
1 |
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|a Zou, Quan-Ming
|e verfasserin
|4 aut
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700 |
1 |
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|a Zuo, Qian-Fei
|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 194(2018) vom: 30. Sept., Seite 1-8
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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773 |
1 |
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|g volume:194
|g year:2018
|g day:30
|g month:09
|g pages:1-8
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|u http://dx.doi.org/10.1016/j.clim.2018.05.007
|3 Volltext
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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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 194
|j 2018
|b 30
|c 09
|h 1-8
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