IFN-α cannot substitute lack of IFN-γ responsiveness in cells of an IFN-γR1 deficient patient

Copyright © 2010 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 138(2011), 3 vom: 02. März, Seite 282-90
1. Verfasser: van de Wetering, Diederik (VerfasserIn)
Weitere Verfasser: van Wengen, Annelies, Savage, Nigel D L, van de Vosse, Esther, van Dissel, Jaap T
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2011
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Interferon-alpha Interleukins Lipopolysaccharide Receptors Lipopolysaccharides Receptors, Interferon STAT1 Transcription Factor STAT1 protein, human Tumor Necrosis Factor-alpha mehr... Interferon-gamma 82115-62-6
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245 1 0 |a IFN-α cannot substitute lack of IFN-γ responsiveness in cells of an IFN-γR1 deficient patient 
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520 |a Patients with complete IFN-γR deficiency are unable to respond to IFN-γ and have impaired Th1-immunity and recurrent, severe infections with weakly virulent Mycobacteria. Since IFN-α and IFN-γ share signalling pathways, treatment with IFN-α has been proposed in complete IFN-γR deficiency. We stimulated cells from healthy controls and from a patient lacking IFN-γR1 with IFN-α and IFN-γ, to establish whether IFN-α would substitute for IFN-γ effects. IFN-α induced STAT1 phosphorylation in monocytes of the IFN-γR1(-/-) patient, but did not prime for LPS-induced IL-12p70, IL-12p40, IL-23 or TNF production. In control cells, IFN-α inhibited the priming effect of IFN-γ on LPS-induced pro-inflammatory cytokine release. Finally, IFN-γ but not IFN-α induced killing of M. smegmatis in cultured macrophages. In conclusion, no evidence was found to support the use of IFN-α in IFN-γR-deficient patients as intervention against mycobacterial infection; on the contrary, treatment of individuals with IFN-α may even adversely affect host defence against Mycobacteria 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 7 |a Interferon-alpha  |2 NLM 
650 7 |a Interleukins  |2 NLM 
650 7 |a Lipopolysaccharide Receptors  |2 NLM 
650 7 |a Lipopolysaccharides  |2 NLM 
650 7 |a Receptors, Interferon  |2 NLM 
650 7 |a STAT1 Transcription Factor  |2 NLM 
650 7 |a STAT1 protein, human  |2 NLM 
650 7 |a Tumor Necrosis Factor-alpha  |2 NLM 
650 7 |a Interferon-gamma  |2 NLM 
650 7 |a 82115-62-6  |2 NLM 
700 1 |a van Wengen, Annelies  |e verfasserin  |4 aut 
700 1 |a Savage, Nigel D L  |e verfasserin  |4 aut 
700 1 |a van de Vosse, Esther  |e verfasserin  |4 aut 
700 1 |a van Dissel, Jaap T  |e verfasserin  |4 aut 
773 0 8 |i Enthalten in  |t Clinical immunology (Orlando, Fla.)  |d 1999  |g 138(2011), 3 vom: 02. März, Seite 282-90  |w (DE-627)NLM098196855  |x 1521-7035  |7 nnns 
773 1 8 |g volume:138  |g year:2011  |g number:3  |g day:02  |g month:03  |g pages:282-90 
856 4 0 |u http://dx.doi.org/10.1016/j.clim.2010.12.005  |3 Volltext 
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