Neuronal Fc gamma receptor I as a novel mediator for IgG immune complex-induced peripheral sensitization

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)2075-2079
Number of pages5
JournalNeural Regeneration Research
Volume7
Issue number26
DOIs
StatePublished - Sep 15 2012

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Keywords

  • Calcium
  • Dorsal root ganglion
  • Fc gamma receptor
  • Immune complex
  • Immunoglobulin G
  • Nonselective cation channel
  • Pain
  • Primary sensory afferents
  • Transient receptor potential canonical 3
  • Voltage-gated calcium channel

ASJC Scopus subject areas

  • Developmental Neuroscience

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