Poster Presentation Australasian Society for Immunology Annual Scientific Meeting 2014

IL-31: New cytokine in the pathogenesis of RA (#310)

Mahshid Naser 1 , Elham Aflaki 1 2 , Eskandar Kamali Sarvestani 3
  1. Rheumatology, Shiraz University of Medical Sciences, Shiraz, Iran
  2. Autoimmune Diseases Research Center, Shiraz University of Medical Sciences, Shiraz, Fars, Iran
  3. Immunology, Shiraz University of Medical Sciences, Shiraz, FARS, Iran

It has been suggested that IL-31/IL-31R signaling is a negative regulatory pathway that specifically limits Th2-dependent cytokine production. Given the fact that rheumatoid arthritis is a Th1/Th17-dependent autoimmune diseases, in the present study the sera and synovial fluid levels of IL-31 was compared between 44 patients with rheumatoid arthritis and 44 sex and aged matched osteoarthritic patients as controls. The levels of IL-31 were measured by commercial ELISA kits. Mean of IL-31 levels in the sera and synovial fluid of RA patients were 35.58±58.26 pg/ml and 16.03±26.71 pg/ml, respectively. While no statistical difference was detected in IL-31 sera levels between patients and OA controls (14.73±9.02 pg/ml, p=0.4), the levels of IL-31 in the synovial fluids of patients were significantly higher than controls (0.67±4.72 pg/ml, p<0.0001). However, no significant correlation was detected between the sera or synovial levels of IL-31 in RA patients and CRP levels or ESR. Interestingly, a significant positive correlation was also detected between the number of involved joints and sera levels of IL-31 (p=0.03). In addition, after categorization of patients according to joints deformity, a significant higher concentration of IL-31 was detected in the sera or synovial fluid of patients with joint deformity (40.21±63.07 pg/ml and 18.27±28.43 pg/ml, respectively) compared with those in patients without deformity (14.72±18.75 pg/ml and 5.96±14.19 pg/ml, respectively; p=0.04 and p=0.01, respectively). In conclusion IL-31 can be considered as a new pro-inflammatory cytokine in the pathogenesis of RA and might be considered as a new target for biologic therapy of RA.