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Regen, T.* ; Isaac, S.* ; Amorim, A.* ; Núñez, N.G.* ; Hauptmann, J.* ; Shanmugavadivu, A.* ; Klein, M.* ; Sankowski, R.* ; Mufazalov, I.A.* ; Yogev, N.* ; Huppert, J.* ; Wanke, F.* ; Witting,M. ; Grill, A.* ; Gálvez, E.J.C.* ; Nikolaev, A.* ; Blanfeld, M.* ; Prinz, I.* ; Schmitt-Kopplin, P. ; Strowig, T.* ; Reinhardt, C.* ; Prinz, M.* ; Bopp, T.* ; Becher, B.* ; Ubeda, C.* ; Waisman, A.*

IL-17 controls central nervous system autoimmunity through the intestinal microbiome.

Sci. Immunol. 6:eaaz6563 (2021)

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Open Access Green as soon as Postprint is submitted to ZB.

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Interleukin-17A- (IL-17A) and IL-17F-producing CD4⁺ T helper cells (T_H17 cells) are implicated in the development of chronic inflammatory diseases, such as multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). T_H17 cells also orchestrate leukocyte invasion of the central nervous system (CNS) and subsequent tissue damage. However, the role of IL-17A and IL-17F as effector cytokines is still confused with the encephalitogenic function of the cells that produce these cytokines, namely, T_H17 cells, fueling a long-standing debate in the neuroimmunology field. Here, we demonstrated that mice deficient for IL-17A/F lose their susceptibility to EAE, which correlated with an altered composition of their gut microbiota. However, loss of IL-17A/F in T_H cells did not diminish their encephalitogenic capacity. Reconstitution of a wild-type-like intestinal microbiota or reintroduction of IL-17A specifically into the gut epithelium of IL-17A/F-deficient mice reestablished their susceptibility to EAE. Thus, our data demonstrated that IL-17A and IL-17F are not encephalitogenic mediators but rather modulators of intestinal homeostasis that indirectly alter CNS-directed autoimmunity.

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Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Gut Microbiota; T-cells; Interleukin-17; Cns; Neutralization; Sequences; Cytokine; Receptor

ISSN (print) / ISBN 2470-9468

e-ISSN 2470-9468

Journal Science immunology

Quellenangaben Volume: 6, Issue: 56, Article Number: eaaz6563

Publisher American Association for the Advancement of Science (AAAS)

Publishing Place Washington, DC

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Research Unit BioGeoChemistry and Analytics (BGC)
CF Metabolomics & Proteomics (CF-MPC)

Grants Center for Molecular Medicine Cologne
Stiftung Rheinland-Pfalz fur Innovation
Hertie Foundation
Sobek Foundation
DFG
Research Center for Immunotherapy (FZI) Mainz
MINECO
MINECO FPI predoctoral fellowship
BMBF
Ministry of Science, Research and Arts, Baden-Wurttemberg (Sonderlinie "Neuroinflammation")
Ernst-Jung Foundation
European Union FP7 Project NeuroKine
Swiss National Science Foundation
National Multiple Sclerosis Society