Peripheral role of cathepsin S in Th1 cell-dependent transition of nerve injury-induced acute pain to a chronic pain state.
MouseOtherC57BL/6 and DBA background, including cathepsin S knockout mice
Model: Peripheral nerve injury-induced neuropathic pain; the specific nerve injury model is not stated in the available text
Genetic deletion or pharmacological inhibition of cathepsin S with Z-FL attenuated the maintenance of tactile allodynia, splenic CD4+ T cell expansion, IFN-gamma positive T cell infiltration of the dorsal spinal cord and microglial proliferation after peripheral nerve injury.
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