Immunoregulation of myelin-specific CD4+ T cell response by neural stem/progenitor cells: role of prostaglandin E2.

The abnormal proliferation and polarization of Th17/Th1 subsets are believed to contribute to the progression of multiple sclerosis. We demonstrated that neural stem cells (NSCs) could inhibit CD4(+)T cells from mice of experimental autoimmune encephalomyelitis to proliferate and polarize into Th17 but promote their apoptosis and to generate regulatory T cells in response to myelin antigen via releasing prostaglandin E2 by activated Th1-derived IFN-γ. The study indicated that NSCs play a negatively regulatory role in T cell responses and provided novel evidence for the therapeutic mechanisms underlying the usage of NSCs to treat autoimmune diseases of central nervous system.