Reducing IgG accumulation via neonatal Fc receptor (FcRn) blockade relieves neuropathic pain

This study investigates a potential new treatment for neuropathic pain by targeting the neonatal Fc receptor (FcRn). Neuropathic pain is often driven by immunoglobulin G (IgG), which accumulates in areas like the spinal cord and dorsal root ganglia (DRG). The researchers hypothesized that blocking FcRn, which is responsible for recycling IgG, would reduce the accumulation of IgG and thus alleviate pain. They used efgartigimod, an FcRn blocker, and genetically modified mice lacking FcRn to test this. The results showed that blocking or deleting FcRn reduced pain in mice with nerve injuries. This suggests that targeting FcRn could be a new way to treat neuropathic pain by reducing IgG accumulation and the resulting inflammation.

• 1
  Efgartigimod, an FcRn blocker, alleviated mechanical allodynia when administered either 7 or 28 days post-CCI.
• 2
  Both systemic (intraperitoneal) and localized (intrathecal) administration of efgartigimod attenuated mechanical allodynia for at least one month.
• 3
  Genetic deletion of FcRn in mice (FcRn−) also reduced CCI-induced allodynia compared to wild-type mice.