Type I IFNs enhance human dorsal root ganglion nociceptor excitability and induce TRPV1 sensitization.

ABSTRACT: Type I interferons (IFNs) are critical cytokines for antiviral defense and are linked to painful diseases like rheumatoid arthritis, lupus, and neuropathic pain in humans. IFN-α therapy can cause myalgia, headache, and joint and abdominal pain. Studies in rodent models demonstrate that direct action of IFNs on sensory neurons in the dorsal root ganglion (DRG) promotes hyperexcitability, but rodent behavioral data on IFNs are conflicting, with reports of both pro- and antinociceptive actions. We sought to clarify the action of IFN-α and IFN-β on human DRG (hDRG) nociceptors. We found that IFN receptor subunits IFNAR1 and IFNAR2 are expressed by these neurons, and their engagement induces canonical STAT1 signaling and noncanonical MAPK activation as measured by increased phosphorylation of t

SUBMITTER: Franco-Enzastiga U 

PROVIDER: S-EPMC12513479 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature