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Origins of rheumatoid arthritis

Author

Boissier MC1, Biton J2, Semerano L3, Decker P2, Bessis N2. Joint Bone Spine. 2019 Dec 5. pii: S1297-319X(19)30175-7. doi: 10.1016/j.jbspin.2019.11.009. [Epub ahead of print]

Author Information

1 Inserm U1125, 93000 Bobigny, France; Université Paris 13, IFRB, Li2P, 93000 Bobigny, France; Service de rhumatologie, hôpital Avicenne, AP-HP, GHUPSSD, 125, rue de Stalingrad, 93000 Bobigny, France. Electronic address: marie-christophe.boissier@aphp.fr.

2 Inserm U1125, 93000 Bobigny, France; Université Paris 13, IFRB, Li2P, 93000 Bobigny, France.

3 Inserm U1125, 93000 Bobigny, France; Université Paris 13, IFRB, Li2P, 93000 Bobigny, France; Service de rhumatologie, hôpital Avicenne, AP-HP, GHUPSSD, 125, rue de Stalingrad, 93000 Bobigny, France.

Abstract

While the exact cause of rheumatoid arthritis is unknown, several mechanisms have been described extensively. The genetic predisposition for this autoimmune disease is largely attributed to MHC class II genes, especially the main polymorphism in the HLA shared epitope. Non-genetic factors account for the rest. The best known are autoantigens to citrullinated or carbmylated proteins, although there are many others. They are recognized by an immune system with defective control mechanisms, in which regulator T-cells are unable to prevent inflammation and the destruction of tissue, joint and vascular structures (among others). Polymorphonuclear neutrophils, which are very abundant at sites of inflammation, interfere with attempts at regulation. Cell metabolism, which typically participates in fighting against the autoantigen attack, does not respond correctly to the demands, making the inflammatory phenomenon worse. This is also the case for environmental factors such as atmospheric pollution, dust, diet (especially salt intake) and infections. Inflammatory cytokines such as TNF-α, IL-1 and IL-17, are certain implicated, but not initially. They appear as a common execution pathway for a lengthy sentence following an unfortunate encounter between genetic predisposition and a harmful environment.