NDLI: The interdependent, overlapping and differential roles of type I and type II interferons in the pathogenesis of experimental autoimmune encephalomyelitis 1

Content Provider	PubMed Central
Author	Naves, Rodrigo Singh, Simer P. Cashman, Kevin S. Rowse, Amber L. Axtell, Robert C. Steinman, Lawrence Mountz, John D. Steele, Chad Sarno, Patrizia De Raman, Chander
Abstract	Type I IFNs (IFN-α and IFN-β) and type II IFN (IFN-γ) mediate both regulation and inflammation in multiple sclerosis (MS), neuromyelitis optica (NMO) and in experimental autoimmune encephalomyelitis (EAE). However the underlying mechanism for these Janus-like activities of type I and II IFNs in neuroinflammation remains unclear. Although endogenous type I IFN-signaling provides a protective response in neuroinflammation, we find that when IFN-γ signaling is ablated, type I IFNs drive inflammation resulting in exacerbated EAE. IFN-γ has disease stage-specific opposing function in EAE. Treatment of mice with IFN-γ during initiation phase of EAE leads to enhanced severity of disease. In contrast, IFN-γ treatment during effector phase attenuated disease. This immunosuppressive activity of IFN-γ required functional type I IFN-signaling. In IFN-α/β receptor (IFNAR) deficient mice, IFN-γ treatment during effector phase of EAE exacerbated disease. Using an adoptive transfer-EAE model, we found that T-cell intrinsic type I and type II IFN signals are simultaneously required to establish chronic EAE by encephalitogenic Th1 cells. However in Th17 cells loss of either IFN signals leads to the development of a severe chronic disease. The data implies that type I and type II IFN signals have independent but non-redundant role in restraining encephalitogenic Th17 cells in vivo. Overall our data show that type I and type II IFNs function in an integrated manner to regulate the pathogenesis in EAE.
Related Links	http://dx.doi.org/10.4049/jimmunol.1300419
Ending Page	2977
Page Count	11
Starting Page	2967
File Format	PDF
ISSN	00221767
e-ISSN	15506606
Journal	Journal of immunology (Baltimore, Md. : 1950)
Issue Number	6
Volume Number	191
Language	English
Publisher Date	2013-09-15
Access Restriction	Open
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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