In a series of prior works, we have established that demyelination contributes to neuropathic pain in part through T cell-mediated autoreactivity of MBP fragments, such as MBP84-104, proteolytically released after a focal nerve trauma (Chernov et al., 2018; Hong et al., 2017; Kobayashi et al., 2008; Liu et al., 2012; Remacle et al., 2018). Here, MBP is linked to injury.