Next Article in Journal
Control of Biofilms with the Fatty Acid Signaling Molecule cis-2-Decenoic Acid
Next Article in Special Issue
The Type I IFN-Induced miRNA, miR-21
Previous Article in Journal
Non-Monotonic Survival of Staphylococcus aureus with Respect to Ciprofloxacin Concentration Arises from Prophage-Dependent Killing of Persisters
Previous Article in Special Issue
Tryptophan Breakdown in Patients with HCV Infection is Influenced by IL28B Polymorphism
Article Menu

Export Article

Open AccessReview
Pharmaceuticals 2015, 8(4), 793-815; doi:10.3390/ph8040793

Therapeutic Potential of Interferon-γ and Its Antagonists in Autoinflammation: Lessons from Murine Models of Systemic Juvenile Idiopathic Arthritis and Macrophage Activation Syndrome

Laboratory of Immunobiology, Department of Microbiology and Immunology, Rega Institute, KU Leuven - University of Leuven, Leuven B-3000, Belgium
*
Author to whom correspondence should be addressed.
Academic Editor: Howard A. Young
Received: 16 October 2015 / Revised: 9 November 2015 / Accepted: 18 November 2015 / Published: 25 November 2015
(This article belongs to the Special Issue Interferons 2015)
View Full-Text   |   Download PDF [749 KB, uploaded 25 November 2015]   |  

Abstract

Interferon-γ (IFN-γ) affects immune responses in a complex fashion. Its immunostimulatory actions, such as macrophage activation and induction of T helper 1-type responsiveness, are widely acknowledged, however, as documented by a large body of literature, IFN-γ has also the potential to temper inflammatory processes via other pathways. In autoimmune and autoinflammatory disorders, IFN-γ can either play a disease-enforcing role or act as protective agent, depending on the nature of the disease. In animal models of any particular autoimmune disease, certain changes in the induction procedure can reverse the net outcome of introduction or ablation of IFN-γ. Here, we review the role of endogenous IFN-γ in inflammatory disorders and related murine models, with a focus on systemic juvenile idiopathic arthritis (sJIA) and macrophage activation syndrome (MAS). In particular, we discuss our recent findings in a mouse model of sJIA, in which endogenous IFN-γ acts as a regulatory agent, and compare with results from mouse models of MAS. Also, we elaborate on the complexity in the activity of IFN-γ and the resulting difficulty of predicting its value or that of its antagonists as treatment option. View Full-Text
Keywords: interferon-γ; therapy; autoinflammation; systemic juvenile idiopathic arthritis; mouse model interferon-γ; therapy; autoinflammation; systemic juvenile idiopathic arthritis; mouse model
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Avau, A.; Matthys, P. Therapeutic Potential of Interferon-γ and Its Antagonists in Autoinflammation: Lessons from Murine Models of Systemic Juvenile Idiopathic Arthritis and Macrophage Activation Syndrome. Pharmaceuticals 2015, 8, 793-815.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Pharmaceuticals EISSN 1424-8247 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top