title: Neuronal Fc gamma receptor I as a novel mediator for IgG immune complex-induced peripheral sensitization.
abstract: Chronic pain often accompanies immune-related diseases with an elevated level of IgG immune complex (IgG-IC) in the serum and/or the affected tissues though the underlying mechanisms are largely unknown. Fc gamma receptors (FcγRs), known as the receptors for the Fc domain of immunoglobulin G (IgG), are typically expressed on immune cells. A general consensus is that the activation of FcγRs by IgG-IC in such immune cells induces the release of proinflammatory cytokines from the immune cells, which may contribute to the IgG-IC-mediated peripheral sensitization. In addition to the immune cells, recent studies have revealed that FcγRI, but not FcγRII and FcγRIII, is also expressed in a subpopulation of primary sensory neurons. Moreover, IgG-IC directly excites the primary sensory neurons through neuronal FcγRI. These findings indicate that neuronal FcγRI provides a novel direct linkage between immunoglobulin and primary sensory neurons, which may be a novel target for the treatment of pain in the immune-related disorders. In this review, we summarize the expression pattern, functions, and the associated cellular signaling of FcγRs in the primary sensory neurons.
authors.affiliation: Department of Anesthesiology, Yale University School of Medicine, New Haven, CT 06510, USA.
authors.forename: Lintao
authors.initials: L
authors.lastname: Qu
keywords: Fc gamma receptor; calcium, immune complex; dorsal root ganglion; immunoglobulin G; nonselective cation channel; pain; primary sensory afferents; transient receptor potential canonical 3; voltage-gated calcium channel