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

8Citations
Citations of this article
14Readers
Mendeley users who have this article in their library.

Abstract

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-γ 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. © 2010 Elsevier Inc.

Cite

CITATION STYLE

APA

de Wetering, D. van, van Wengen, A., Savage, N. D. L., van de Vosse, E., & van Dissel, J. T. (2011). IFN-γ cannot substitute lack of IFN-γ responsiveness in cells of an IFN-γR1 deficient patient. Clinical Immunology, 138(3), 282–290. https://doi.org/10.1016/j.clim.2010.12.005

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free