Abstract
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.
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