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PRECLINICAL PUBLICATION · 2014

Peripheral role of cathepsin S in Th1 cell-dependent transition of nerve injury-induced acute pain to a chronic pain state.

Mouse / Other

Evidence by therapy association

Study details and outcomes are extracted in the context of a specific intervention. Separate associations are retained rather than silently merged.

PMID 24553941 ↗2014Reported benefit

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.

Extraction: extract · Supplied extraction confidence: 0.55. Machine-extracted fields require source verification.