Friday, September 23rd
B Cell Regulation of Neuropathic Pain
Our unbiased transcriptome screens suggested that enhanced B cell signaling is an under-appreciated consequence of injury. New data will be presented to demonstrate that B cells are necessary for initiation of neuropathic pain. We show that constitutive deficiency or pharmacological depletion of B cells protects male and female mice from neuropathic pain. As the key mechanism, antibodies secreted by differentiated B cells form complexes with autoantigens induced by the sterile injury, and activate Fc gamma receptors along the pain neuraxis. Moreover, evidence for elevated antibodies in CSF of patients with neuropathic pain will be presented. Together, these data implicate a new, clinically-relevant cell-signaling axis in maintaining pain after traumatic nerve injury.