DLK mediates the neuronal intrinsic immune response and regulates glial reaction and neuropathic pain

摘要: Inflammatory response triggered by nerve injury plays important roles in the development of neurological disorders, such as neuropathic pain. The signaling events leading to inflammation nervous system remain poorly understood. Here, deleting Dlk sensory neurons driven Wnt1a-Cre, we show that dual leucine zipper kinase (DLK) is required for neuronal intrinsic immune induce cytokines and chemokines Ccl2, Ccl7, Ccl12 upon injury. DLK-controlled could regulate CD11b+ cell infiltration dorsal root ganglia, well microgliosis astrogliosis spinal horn but not ventral horn. Deficiency drastically alleviates pain elicited chronic constriction sciatic nerve. Thus, DLK an essential component mediates regulates cord.