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Regen, Tommy; Isaac, Sandrine; Amorim, Ana; Núñez, Nicolás Gonzalo; Hauptmann, Judith; Shanmugavadivu, Arthi; Klein, Matthias; Sankowski, Roman; Mufazalov, Ilgiz A; Yogev, Nir; Huppert, Jula; Wanke, Florian; Witting, Michael; Grill, Alexandra; Gálvez, Eric J C; Nikolaev, Alexei; Blanfeld, Michaela; Prinz, Immo; Schmitt-Kopplin, Philippe; Strowig, Till; Reinhardt, Christoph; Prinz, Marco; Bopp, Tobias; Becher, Burkhard; Ubeda, Carles; Waisman, Ari
Science immunology, 02/2021, Letnik: 6, Številka: 56Journal Article
Interleukin-17A- (IL-17A) and IL-17F-producing CD4 T helper cells (T 17 cells) are implicated in the development of chronic inflammatory diseases, such as multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). T 17 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 17 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 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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