IL-10, IL-4, and STAT6 promote an M2 milieu required for termination of P0(106-125)-induced murine experimental autoimmune neuritis.

The role of the type 2 helper T cell (Th2)-polarizing cytokines IL-4 and IL-10 has not yet been studied in P0106-125-induced murine experimental autoimmune neuritis (EAN). We, therefore, addressed the functional relevance of these cytokines and signaling via the IL-4-associated transcription factor STAT6. The clinical course of P0106-125-induced EAN in mice deficient for IL-10(0/0), IL-4(0/0), or STAT6(0/0) was significantly aggravated compared with that of wild-type control mice.