Endogenous ligands present in the injured and inflamed system activate resident TLRs, localized to glia and/or neurons. Based on the effects of IT TLR ligands, it is hypothesized that TLRs signaling through TIRAP and MyD88 lead to NFκB mediated cytokine (TNF) release and to a TNF dependent allodynia (e.g. TLR2 and TLR4). However, TLR3 leads to a TNF independent allodynia and IFNβ production. Based on the effects of Ifnar−/− mice, the increased IFNβ production regulates the allodynic actions mediated by TIRAP (TLR2/TLR4 activation) and induced by IT TLR3-L. As TLR4 activated both TRIF and TIRAP signaling, the net allodynic effect reflects the facilitation mediated by spinal TNF release and the inhibition initiated by TRIF mediated IFNβ production.