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Citations to this article

IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation in mice
Stefan Haak, … , Burkhard Becher, Ari Waisman
Stefan Haak, … , Burkhard Becher, Ari Waisman
Published December 15, 2008
Citation Information: J Clin Invest. 2009;119(1):61-69. https://doi.org/10.1172/JCI35997.
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Research Article Autoimmunity Article has an altmetric score of 10

IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation in mice

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Abstract

The clear association of Th17 cells with autoimmune pathogenicity implicates Th17 cytokines as critical mediators of chronic autoimmune diseases such as EAE. To study the impact of IL-17A on CNS inflammation, we generated transgenic mice in which high levels of expression of IL-17A could be initiated after Cre-mediated recombination. Although ubiquitous overexpression of IL-17A led to skin inflammation and granulocytosis, T cell–specific IL-17A overexpression did not have a perceptible impact on the development and health of the mice. In the context of EAE, neither the T cell–driven overexpression of IL-17A nor its complete loss had a major impact on the development of clinical disease. Since IL-17F may be able to compensate for the loss of IL-17A, we also generated IL-17F–deficient mice. This strain was fully susceptible to EAE and displayed unaltered emergence and expansion of autoreactive T cells during disease. To eliminate potential compensatory effects of either cytokine, we treated IL-17F–deficient mice with antagonistic monoclonal antibodies specific for IL-17A and found again only a minimal beneficial impact on disease development. We conclude therefore that both IL-17A and IL-17F, while prominently expressed by an encephalitogenic T cell population, may only marginally contribute to the development of autoimmune CNS disease.

Authors

Stefan Haak, Andrew L. Croxford, Katharina Kreymborg, Frank L. Heppner, Sandrine Pouly, Burkhard Becher, Ari Waisman

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Total citations by year

Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 Total
Citations: 2 5 7 6 13 10 13 7 7 20 17 15 15 19 23 27 15 221
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Citations to this article in year 2017 (7)

Title and authors Publication Year
GM-CSF is not essential for experimental autoimmune encephalomyelitis but promotes brain-targeted disease
Emily Pierson, Joan Goverman
JCI Insight 2017
IL-23R-activated STAT3/STAT4 is essential for Th1/Th17-mediated CNS autoimmunity
Priscilla Lee, Alan Smith, Yuhong Yang, Selhorst Amanda, Yue Liu, Michael Racke, Amy Lovett-Racke
JCI Insight 2017
GM-CSF Promotes Chronic Disability in Experimental Autoimmune Encephalomyelitis by Altering the Composition of Central Nervous System–Infiltrating Cells, but Is Dispensable for Disease Induction
PC Duncker, JS Stoolman, AK Huber, BM Segal
Journal of immunology (Baltimore, Md. : 1950) 2017
Differentiation and Transmigration of CD4 T Cells in Neuroinflammation and Autoimmunity
SA Sonar, G Lal
Frontiers in immunology 2017
Clinical and Histopathological Amelioration of Experimental Autoimmune Encephalomyelitis by AAV Vectors Expressing a Soluble Interleukin-23 Receptor
M Miralles, H Eixarch, M Tejero, C Costa, K Hirota, AR Castaño, M Puig, G Stockinger, X Montalban, A Bosch, C Espejo, M Chillon
Neurotherapeutics 2017
Avoiding contact allergens: from basic research to the in vitro identification of contact allergens
SF Martin, PR Esser
2017
Novel key cytokines in allergy: IL-17, IL-22
S Eyerich, C Traidl-Hoffmann, H Behrendt, A Cavani, CB Schmidt-Weber, J Ring, K Eyerich
2017

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