Immunodominant fragments of myelin basic protein initiate T cell-dependent pain
Journal of Neuroinflammation, 06/08/2012
Liu H et al. – The data implicate myelin basic protein (MBP) as a novel mediator of pain. Furthermore, the action of matrix metalloproteinases (MMPs) expressed within 1 day post–injury is critical to the generation of tactile allodynia, neuroinflammation, and the immunodominant MBP digest peptides in nerve. These MBP peptides initiate mechanical allodynia in both a T cell–dependent and –independent manner. In the course of Wallerian degeneration, the repeated exposure of the cryptic MBP epitopes, which are normally sheltered from immunosurveillance, may induce the MBP–specific T cell clones and a self–sustaining immune reaction, which may together contribute to the transition of acute pain into a chronic neuropathic pain state.