Reducing IgG accumulation via neonatal Fc receptor (FcRn) blockade relieves neuropathic pain
Nathan T. Fiore, Kendal F. Willcox, Dorsa Dayani, Younus A. Zuberi, Cobi J. Heijnen, Peter M. Grace
Abstract
mice post-CCI compared to controls. The FcRγ subunit is a key component of Fc gamma receptors (FcγRs), which are activated by IgG immune complexes. In macrophage cultures stimulated by IgG immune complexes, FcRn blockade also dampened FcγR-dependent production of proinflammatory cytokines. Collectively, our study demonstrates that FcRn blockade or deletion alleviates mechanical allodynia and reduces IgG accumulation after CCI, attenuating pronociceptive IgG-FcγR signaling around the lumbar region. Strategies to block FcRn and reduce IgG recycling warrant further investigation as potential treatments for IgG-mediated neuropathic pain.
Topics & Concepts
BlockadeNeuropathic painNeonatal Fc receptorMedicineReceptorPharmacologyChemistryImmunoglobulin GAnesthesiaAntibodyImmunologyInternal medicineNeuropeptides and Animal PhysiologyReceptor Mechanisms and SignalingAdenosine and Purinergic Signaling