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  Gene Expression in Spontaneous Experimental Autoimmune Encephalomyelitis Is Linked to Human Multiple Sclerosis Risk Genes

Faber, H., Kurtoic, D., Krishnamoorthy, G., Weber, P., Puetz, B., Mueller-Myhsok, B., et al. (2020). Gene Expression in Spontaneous Experimental Autoimmune Encephalomyelitis Is Linked to Human Multiple Sclerosis Risk Genes. Frontiers in immunology, 11: 2165. doi:10.3389/fimmu.2020.02165.

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© 2020 Faber, Kurtoic, Krishnamoorthy, Weber, Pütz, Müller-Myhsok, Weber and Andlauer.

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The Supplementary Material for this article can be found online at:

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 Creators:
Faber, Hans1, Author
Kurtoic, Dunja1, Author
Krishnamoorthy, Gurumoorthy2, Author              
Weber, Peter1, Author
Puetz, Benno1, Author
Mueller-Myhsok, Bertram1, Author
Weber, Frank1, Author
Andlauer, Till F. M.1, Author
Affiliations:
1external, ou_persistent22              
2Krishnamoorthy, Gurumoorthy / Neuroinflammation and Mucosal Immunology, Max Planck Institute of Biochemistry, Max Planck Society, ou_2173635              

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Free keywords: T-CELL RESPONSES; MICROBIOTA; MODELSImmunology; experimental autoimmune encephalomyelitis (EAE); myelin oligodendrocyte glycoprotein (MOG); T helper cell (Th); multiple sclerosis; risk genes; gene expression;
 Abstract: Recent genome-wide association studies have identified over 230 genetic risk loci for multiple sclerosis. Current experimental autoimmune encephalomyelitis (EAE) models requiring active induction of disease may not be optimally suited for the characterization of the function of these genes. We have thus used gene expression profiling to study whether spontaneous opticospinal EAE (OSE) or MOG-induced EAE mirrors the genetic contribution to the pathogenesis of multiple sclerosis more faithfully. To this end, we compared gene expression in OSE and MOG EAE models and analyzed the relationship of both models to human multiple sclerosis risk genes and T helper cell biology. We observed stronger gene expression changes and an involvement of more pathways of the adaptive immune system in OSE than MOG EAE. Furthermore, we demonstrated a more extensive enrichment of human MS risk genes among transcripts differentially expressed in OSE than was the case for MOG EAE. Transcripts differentially expressed only in diseased OSE mice but not in MOG EAE were significantly enriched for T helper cell-specific transcripts. These transcripts are part of immune-regulatory pathways. The activation of the adaptive immune system and the enrichment of both human multiple sclerosis risk genes and T helper cell-specific transcripts were also observed in OSE mice showing only mild disease signs. These expression changes may, therefore, be indicative of processes at disease onset. In summary, more human multiple sclerosis risk genes were differentially expressed in OSE than was observed for MOG EAE, especially in T(H)1 cells. When studying the functional role of multiple sclerosis risk genes and pathways during disease onset and their interactions with the environment, spontaneous OSE may thus show advantages over MOG-induced EAE.

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Language(s): eng - English
 Dates: 2020-09
 Publication Status: Published online
 Pages: 12
 Publishing info: -
 Table of Contents: Data Availability Statement
The datasets presented in this study can be found in online repositories. The names of the repository and accession number(s) can be found at: https://www.ebi.ac.uk/arrayexpress/, E-MTAB-9132; https://www.ebi.ac.uk/arrayexpress/, E-MTAB-9133.
 Rev. Type: Peer
 Identifiers: ISI: 000576462100001
DOI: 10.3389/fimmu.2020.02165
 Degree: -

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Project name : GAMES; 635617
Grant ID : 635617
Funding program : starting grant
Funding organization : European Research Council
Project name : SFB TR-128 (Project A1)
Grant ID : -
Funding program : -
Funding organization : German research foundation

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Title: Frontiers in immunology
  Abbreviation : Front immunol
Source Genre: Journal
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Publ. Info: Lausanne : Frontiers Media
Pages: - Volume / Issue: 11 Sequence Number: 2165 Start / End Page: - Identifier: ISSN: 1664-3224
CoNE: https://pure.mpg.de/cone/journals/resource/1664-3224