Article Text

AB0351 1,25-dihydroxyvitamin d3 inhibits the rankl pathway and impacts on the production of pathway-associated cytokines in early rheumatoid arthritis
  1. J. Luo1,
  2. X. Li1
  1. 1Division of rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, P. R. China, Taiyuan, China


Background Rheumatoid arthritis (RA) was a common chronic autoimmune disorder characterized with synovial inflammation. Bone loss in the inflamed joints occurred in the early stage of the disease, followed by the destruction of articular cartilage and bones. During the processing of the disease, the signaling pathway of receptor activator of nuclear factor kappa-B ligand (RANKL) and osteoprotegerin (OPG) was crucial in osteoclasts differentiation and activation.

Objectives To study effects of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on RANKL signaling pathway and pathway-associated cytokines in patients with rheumatoid arthritis (RA).

Methods Receptor activator of nuclear factor-kappa B ligand (RANKL), osteoprotegerin (OPG), IFN-γ, IL-6, TNF-α, IL-17 and IL-4 were examined in 54 patients with active RA using a cytometric bead array (CBA) and an enzyme-linked immunosorbent assay (ELISA).

Results After 72 hours of incubation of peripheral blood mononuclear Cell (PBMC) with 1,25(OH)2D3, the levels of RNAKL, TNF-α, IL-17 and IL-6 significantly decreased. 1,25(OH)2D3 had no significantly impact on the level of OPG, RANKL/OPG and IL-4. The ratios of IL-17/IL-4, TNF-α/IL-4, IFN-γ/IL-4 significantly decreased in 1,25(OH)2D3 testing groups.

Conclusions The present study demonstrated that 1,25(OH)2D3 reduces the production of RANKLE and the secretion of TNF-α, IL-17, and IL-6 in PBMC of RA patients, which indicates that 1,25(OH)2D3 might be able to decrease damage of cartilage and bone in RA patients by regulating the expression of RANKL signaling pathway and pathway-associated cytokines.

References Disclosure of Interest: None Declared

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