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- W3136284627 endingPage "e905" @default.
- W3136284627 startingPage "e905" @default.
- W3136284627 abstract "In Brief Chronic pain is an unpleasant and debilitating condition that is often poorly managed by existing therapeutics. Reciprocal interactions between the nervous system and the immune system have been recognized as playing an essential role in the initiation and maintenance of pain. In this review, we discuss how neuroimmune signaling can contribute to peripheral and central sensitization and promote chronic pain through various autoimmune mechanisms. These pathogenic autoimmune mechanisms involve the production and release of autoreactive antibodies from B cells. Autoantibodies—ie, antibodies that recognize self-antigens—have been identified as potential molecules that can modulate the function of nociceptive neurons and thereby induce persistent pain. Autoantibodies can influence neuronal excitability by activating the complement pathway; by directly signaling at sensory neurons expressing Fc gamma receptors, the receptors for the Fc fragment of immunoglobulin G immune complexes; or by binding and disrupting ion channels expressed by nociceptors. Using examples primarily from rheumatoid arthritis, complex regional pain syndrome, and channelopathies from potassium channel complex autoimmunity, we suggest that autoantibody signaling at the central nervous system has therapeutic implications for designing novel disease-modifying treatments for chronic pain. Autoantibodies can contribute to peripheral and central sensitization through activation of complement pathway, activation of neuronal Fc gamma receptors, and disrupted function of neuronal ion channels." @default.
- W3136284627 created "2021-03-29" @default.
- W3136284627 creator A5007674783 @default.
- W3136284627 creator A5025282582 @default.
- W3136284627 creator A5025955142 @default.
- W3136284627 creator A5091505369 @default.
- W3136284627 date "2021-01-01" @default.
- W3136284627 modified "2023-10-14" @default.
- W3136284627 title "Autoimmune regulation of chronic pain" @default.
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