The motorized RhoGAP myosin IXb (Myo9b) in leukocytes regulates experimental autoimmune encephalomyelitis induction and recovery

• Myo9b−/− mice showed a delayed initiation of active EAE and lack of recovery.
• Myo9b−/− mice had a delayed infiltration of Th1 and Th17 cells to the CNS.
• Th17 cells and CD11b + macrophages remain elevated in the CNS of Myo9b−/− mice.
• Myo9b in leukocytes regulates the course of EAE.

Myo9b regulates leukocyte migration by controlling RhoA signaling. Here we assessed its role in active experimental autoimmune encephalomyelitis (EAE). Myo9b−/− mice show a delay in the onset of EAE symptoms. The delay in disease onset was accompanied by reduced numbers of Th1 and Th17 cells in the CNS. Myo9b−/− mice showed no recovery from disease symptoms and exhibited elevated numbers of both Th17 cells and CD11b + macrophages. Bone marrow chimeric mice demonstrated that the absence of a leukocyte source of Myo9b was responsible for the delayed leukocyte infiltration into the CNS, delayed EAE onset and lack of recovery.