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Published in: Journal of NeuroVirology 6/2012

01-12-2012

Possible role of interleukin-17 in a prime/challenge model of multiple sclerosis

Authors: Jane E. Libbey, Ikuo Tsunoda, Robert S. Fujinami

Published in: Journal of NeuroVirology | Issue 6/2012

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Abstract

No one single pathogen has been identified as the causative agent of multiple sclerosis (MS). Alternately, the likelihood of an autoimmune event may be nonspecifically enhanced by different infectious agents. In a novel animal model of MS, SJL/J mice primed through infection with a recombinant vaccinia virus (VV) encoding myelin proteolipid protein (PLP) (VVPLP) were susceptible to a central nervous system (CNS) inflammatory disease following administration of a nonspecific immunostimulant [complete Freund’s adjuvant (CFA) plus Bordetella pertussis (BP)]. Mononuclear cells isolated from the brains, but not the spleens, of VVPLP-primed CFA/BP challenged mice produced interleukin (IL)-17 and interferon-γ and transferred a CNS inflammatory disease to naïve SJL/J mice. Administration of curdlan, a T helper 17 cell inducer, unexpectedly resulted in less severe clinical and histological signs of disease, compared to CFA/BP challenged mice, despite the induction of IL-17 in the periphery. Further examination of the VVPLP-prime CFA/BP challenge model may suggest new mechanisms for how different pathogens associated with MS can protect or enhance disease.
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Metadata
Title
Possible role of interleukin-17 in a prime/challenge model of multiple sclerosis
Authors
Jane E. Libbey
Ikuo Tsunoda
Robert S. Fujinami
Publication date
01-12-2012
Publisher
Springer US
Published in
Journal of NeuroVirology / Issue 6/2012
Print ISSN: 1355-0284
Electronic ISSN: 1538-2443
DOI
https://doi.org/10.1007/s13365-012-0125-y

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