Figure 1. Enforced public TCRβ expression leads to spontaneous autoimmune encephalomyelitis.

TCRβ^−/− Foxp3-GFP HPCs were transduced with TCRβ1 to generate retrogenic mice. (A) Kaplan Meier analysis of overall and disease-free survival. (B) Absolute number of CD4⁺TCR⁺ and CD4⁺TCR⁺Foxp3-GFP⁺ T cells in spleen and CNS of TCRβ1 mice with EAE. (C) Proliferation of splenic T cells from TCRβ1 or control retrogenic mice expressing the OTII TCRβ chain in response to MOG_35-55 or mitogen measured by ³H-thymidine incorporation. (D) Percent of CNS- infiltrating TCRβ1T cells expressing IL-17, IFN-γ, or both IL-17 and IFN-γ in the absence or presence of ex vivo restimulation as determined by intracellular cytokine staining. (E,F) Histologic analyses of the CNS of TCRβ1 retrogenic mice showing a mixed infiltrate of lymphocytes, macrophages, and granulocytes, gliosis and perivascular cuffing in the septum, meninges, and optic nerve (E) and white tracts of the lumbar spinal cord (F) on day 28 of TCRβ1 but not OTIIβ control retrogenic mice. **p ≤ 0.01; ****p ≤ 0.0001.