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Oxysterols regulate encephalitogenic CD4+ T cell trafficking during central nervous system autoimmunity

Chalmin, F., Rochemont, V., Lippens, C., Clottu, A., Sailer, A.W., Merkler, D., Hugues, S., Pot, C.·2015·Journal of Autoimmunity
DOI 10.1016/j.jaut.2014.10.001
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Abstract

Perturbation of steroids pathways is linked to inflammation and chronic diseases, however the underlying mechanism remains unclear. Oxysterols, oxidized forms of cholesterol, are not only essential for bile synthesis and sterol transportation but have recently been shown to contribute to the immune response. In addition, serum oxysterols levels have been proposed as suitable candidate biomarkers for neurological diseases such as multiple sclerosis (MS). However how oxysterols modulate adaptive immunity is unknown and their functions in autoimmunity have not been investigated. The enzyme cholesterol 25 hydroxylase (Ch25h) is the rate limiting step to synthesize the oxysterol 7α,25-dihydroxycholesterol (7α,25-OHC) from cholesterol. We here report, using the MS murine model experimental autoimmune encephalomyelitis (EAE), that Ch25h deletion significantly attenuated EAE disease course by limiting trafficking of pathogenic CD4(+) T lymphocytes to the central nervous system (CNS). Mechanistically, we show a critical involvement for oxysterols in recruiting leukocytes into inflamed tissues and propose that 7α,25-OHC preferentially promotes the migration of activated CD44(+)CD4(+) T cells by binding the G protein-coupled receptor called Epstein-Barr virus induced gene 2 (EBI2). Collectively, our results support a pro-inflammatory role for oxysterols during EAE and identify oxysterols as a potential therapeutic target to treat autoimmune diseases.

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Crossref · 10.1016/j.jaut.2014.10.001

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  • CH25H deficient mice have decreased inflammatory-mediated pathology and death following influenza infection, reduced immune responses following experimental autoimmune encephalomyelitis (EAE), and in a mouse model of X-linked adrenoleukodystrophy (X-ALD).

    “CH25H deficient mice have also been shown to have decreased inflammatory-mediated pathology and death following influenza infection [80], reduced immune responses both following experimental autoimmune encephalomyelitis (EAE) [81] and in a mouse model of X-linked adrenoleukodystrophy (X-ALD) [82]”

    From 25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner (2020) · cites this paper as [81]

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Research works printed but not linked: 32

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Metadata

Authors
Chalmin, F., Rochemont, V., Lippens, C., Clottu, A., Sailer, A. W., Merkler, D., Hugues, S., & Pot, C.
Venue
Journal of Autoimmunity
Publisher
Elsevier BV
Published
2015-01
Volume
56
Pages
45-55
ISSN
0896-8411
DOI
10.1016/j.jaut.2014.10.001
Cited by
98
References
4
Language
en
Licence
Funders
  • Swiss National Science Foundation (310030_138430)
  • FP7-PEOPLE-CIG (293615)
  • Novartis Foundation for Medical-Biological Research (# 11A23)
  • Swiss Multiple Sclerosis Society
  • Klaus-Tschira Foundation
  • Gebert Rüf Stiftung

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