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. Author manuscript; available in PMC: 2009 Jan 1.
Published in final edited form as: Immunity. 2007 Dec 27;28(1):29–39. doi: 10.1016/j.immuni.2007.11.016

Figure 7. RORα and RORγ compound mutations completely inhibit TH17 differentiation in vivo.

Figure 7

(A) Lamina propria cells were isolated from Rag1−/− mice reconstituted with RORαsg/sg, RORγ−/− RORαsg/sg−/− or WT bone marrow cells and IL-17 expression was assessed by intracellular staining. Student t test, *, p<0.05; **, p<0.005. (B) EAE was induced in the indicated Rag1-deficient mice reconstituted with indicated bone marrow cells. WT, n=5; RORγ−/−, n=4; RORαsg/sg−/−, n=5. Max disease, score ≥ 3. *, student t test RORαsg/sg−/− vs WT, p<0.001; RORαsg/sg−/− vs RORγ−/−, p<0.05. Infiltrates in central nerve system or splenocytes from the EAE mice were isolated on day 13 after the 2nd immunization and IL-17- or IFN-γ- expressing cells were measured by intracellular staining. Data shown are on gated CD4+ cells.