BJ-3105 treatment suppresses development of EAE by decreasing autoreactive Th1 and Th17 generation.

<p>Active EAE was elicited in 8–12 weeks female C57BL/6 mice by immunization with MOG_35-55. The mice were subcutaneously treated with vehicle or BJ-3105 (3 mg/kg/every other day) from day 1 post-immunization as detailed under materials and methods. Mice were monitored for signs and symptoms of EAE. (A) Clinical score were recorded every day. (B) Total cell count in spleen and CNS of drug treated and untreated EAE mice. (C) At 24 days after challenge, total mononuclear cell obtained from the brains and spinal cord of MOG_35–55 immunized wild-type mice and BJ-3105-treated mice. Total percent of infiltrated CD4⁺ T cells and CD8⁺ T cells in CNS. (D) After 24 days of EAE, lymphocytes were isolated from the spleen, lymph nodes and spinal cord of mice. The fraction of IFN-γ and IL-17A producing CD4⁺ T cells from spleen, draining lymph node and CNS were determined by intracellular staining and analyzed by flow cytometry. Percentage of Th1 and Th17 cells were shown. (E) Flow cytometry analysis of CXCR3 expression on activated T cells under Th1 and CCR6 expression under Th17-polarizing conditions with or without BJ-3105 (1 μM). Bar diagram showing the mean fluorescence intensity (MFI) of CXCR3 and CCR6. Mean±SEM of multiple mice are shown. <i>*p</i> < 0.05, compared with drug untreated group.