IL-17 controls central nervous system autoimmunity through the intestinal microbiome
Tommy Regen, Sandrine Isaac, Ana Amorim, Nicolás Gonzalo Núñez, Judith Hauptmann, Arthi Shanmugavadivu, Matthias Klein, Roman Sankowski, Ilgiz A. Mufazalov, Nir Yogev, Jula Huppert, Florian Wanke, Michael Witting, Alexandra Grill, Eric J. C. Gálvez, Alexei Nikolaev, Michaela Blanfeld, Immo Prinz, Philippe Schmitt‐Kopplin, Till Strowig, Christoph Reinhardt, Marco Prinz, Tobias Bopp, Burkhard Becher, Carles Úbeda, Ari Waisman
Abstract
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.