Autoantibodies to citrullinated proteins induce joint pain independent of inflammation via a chemokine-dependent mechanism.

Gustaf WigerbladDuygu B BasCátia Fernades-CerqueiraAkilan KrishnamurthyKutty Selva NandakumarKatarzyna RogozJungo KatoKatalin SandorJie SuJuan Miguel Jimenez-AndradeAnja FinnAlex Bersellini FarinottiKhaled AmaraKarin LundbergRikard HolmdahlPer-Johan JakobssonVivianne MalmströmAnca I CatrinaLars KlareskogCamilla I Svensson

Published in: Annals of the rheumatic diseases (2015)

The data suggest that CXCL1/IL-8, released from osteoclasts in an autoantibody-dependent manner, produces pain by activating sensory neurons. The identification of this new pain pathway may open new avenues for pain treatment in RA and also in other painful diseases associated with autoantibody production and/or osteoclast activation.

Keyphrases

chronic pain
pain management
neuropathic pain
rheumatoid arthritis
spinal cord
oxidative stress
systemic lupus erythematosus
spinal cord injury
artificial intelligence
disease activity
postoperative pain
idiopathic pulmonary fibrosis
smoking cessation
interstitial lung disease