The present studies uncovered three important roles of the TLR pathway in mononeuropathy in the male mouse: i) individual TLRs only modestly contribute to the allodynia present after nerve injury; ii) TRIF plays a dual role mediating allodynia arising from TLR3 activation and regulating, through an IFNβ pathway, the recovery following nerve injury-induced allodynia; and iii) the MyD88 pathway is required for the development of contralateral allodynia. Here, MYD88 is linked to mononeuropathy.