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231224s2012 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2012.09.004
|2 doi
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|a pubmed24n0740.xml
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|a (DE-627)NLM222201142
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|a (NLM)23108090
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|a (PII)S1521-6616(12)00229-X
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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 Berthet, Julien
|e verfasserin
|4 aut
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|a Human platelets can discriminate between various bacterial LPS isoforms via TLR4 signaling and differential cytokine secretion
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|c 2012
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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 17.01.2013
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|a Date Revised 16.08.2019
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|a published: Print-Electronic
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|a CommentIn: Clin Immunol. 2013 Jan;146(1):13-4. - PMID 23168607
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|a Citation Status MEDLINE
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|a Copyright © 2012 Elsevier Inc. All rights reserved.
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|a Platelets are currently acknowledged as cells of innate immunity and inflammation and play a complex role in sepsis. We examined whether different types of LPS have different effects on the release of soluble signaling/effective molecules from platelets. We used platelet-rich plasma from healthy volunteers and LPS from two strains of gram-negative bacteria with disparate LPS structures. We combined LPS-stimulated platelet supernatants with reporter cells and measured the PBMC cytokine secretion profiles. Upon stimulation of platelets with both Escherichia coli O111 and Salmonella minnesota LPS, the platelet LPS::TLR4 interaction activated pathways to trigger the production of a large number of molecules. The different platelet supernatants caused differential PBMC secretion of IL-6, TNFα, and IL-8. Our data demonstrate that platelets have the capacity to sense external signals differentially through a single type of pathogen recognition receptor and adjust the innate immune response appropriately for pathogens exhibiting different types of 'danger' signals
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|a Comparative Study
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a CD63 protein, human
|2 NLM
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|a CXCL8 protein, human
|2 NLM
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|a Cytokines
|2 NLM
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|a IL6 protein, human
|2 NLM
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|a Interleukin-6
|2 NLM
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|a Interleukin-8
|2 NLM
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|a Lipopolysaccharide Receptors
|2 NLM
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|a Lipopolysaccharides
|2 NLM
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|a P-Selectin
|2 NLM
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|a Protein Isoforms
|2 NLM
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|a SELP protein, human
|2 NLM
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|a TLR4 protein, human
|2 NLM
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|a Tetraspanin 30
|2 NLM
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|a Toll-Like Receptor 4
|2 NLM
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|a Tumor Necrosis Factor-alpha
|2 NLM
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|a Damien, Pauline
|e verfasserin
|4 aut
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|a Hamzeh-Cognasse, Hind
|e verfasserin
|4 aut
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|a Arthaud, Charles-Antoine
|e verfasserin
|4 aut
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|a Eyraud, Marie-Ange
|e verfasserin
|4 aut
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|a Zéni, Fabrice
|e verfasserin
|4 aut
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|a Pozzetto, Bruno
|e verfasserin
|4 aut
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|a McNicol, Archibald
|e verfasserin
|4 aut
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|a Garraud, Olivier
|e verfasserin
|4 aut
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|a Cognasse, Fabrice
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 145(2012), 3 vom: 14. Dez., Seite 189-200
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:145
|g year:2012
|g number:3
|g day:14
|g month:12
|g pages:189-200
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|u http://dx.doi.org/10.1016/j.clim.2012.09.004
|3 Volltext
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|a AR
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|d 145
|j 2012
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|h 189-200
|