IL-23 is absolutely crucial for the development of T-cell driven autoimmune disease in mice. Even though IL-23 is widely held to be involved in the stabilization of IL-17-secreting T cells, naïve T cells lack the IL-23 receptor. Thus, the primary cellular target of IL-23 in the context of autoimmunity is a subject of some debate. Innate lymphoid cells (ILCs) are a recently discovered family of lymphocytes being involved in early host defense, particularly at mucosal epithelial surfaces. Given the fact that RORγt-dependent ILCs (group 3 ILCs) constitutively express the IL-23-receptor, and that they have been implicated in intestinal autoimmunity, we hypothesized that ILCs could contribute to the early development of autoimmune neuroinflammation. Through systematic analysis, we detected a sizable population of Thy1(+) Sca1(+) ILCs in the inflamed CNS tissue. CNS-infiltrating ILCs were characterized by expression of the IL-7-receptor and production of proinflammatory IL-17 and IFN-γ. Furthermore, genetic fate-mapping revealed their dependence on the transcription factor RORγt. However, upon specific in vivo ablation of this cell population, we found that they do not influence the course of the disease.