A longitudinal study to investigate the role of il-6 and il 17 in the pathogenesis of early rheumatoid arthritis

الملخص EN

Background : previous researches indicate that IL-6 is a pro-inflammatory cytokine in RA that can drive Thl7 cell development in mice and humans.

Data from experimental arthritis models suggest that Thl7 cells are pathogenic via production of the pro-inflammatory cytokines IL-17 and TNFa, leading to monocyte and fibroblast activation, and involvement in osteoclastogeneis and joint damage.

Objectives : the aim of this study is to investigate if interleukin-6 (IL-6) and/or interleukin-17 (IL-17) and Th 17 cells are biomarkers for disease progression and severity in early Undifferentiated Arthritis (UA) andRheumatoid Arthritis(RA) patients.

Methods : we performed a longitudinal study recruiting 20 patients with either undifferentiated inflammatory arthritis or early rheumatoid arthritis.

We also recruited 30 age (mean = 46) and sex-matched healthy controls The patients were assessed at baseline, 6 and 12 months for the American College of Rheumatology (ACR) criteria, Rheumatoid factor (RF), Anti Citrullinated Peptides (Anti-CCP), ESR, CRP, X-Rayofthe hands and feet, joint count, patient global assessment, DAS28 and Quality of Life (HAQ) measurements.

Peripheral blood and serum samples were taken and PBMC isolated.

Cell subset analysis (CD3, CD4 / CD8, and CD14) was performed ex vivo.

Results : peripheral blood monocytes In RA and UDA showed the proportion of IL6 CD14 + Monocytes significantly higher in RA patients at base line than the UDA.

sero-postive patients were higher in the proportion of (Total IL17 CD3 + CD4 + Tcells, IFNy + IL17+ CD3 + CD4 + Tcells, IL6 CD 14+Monocytes) than the sero-negative patients but that differences did not reach statistical significance.

The longitudinal follow up for the early arthritis group, showed a significant change in the % IL6 Monocytes.

Conclusions : the proportion ofIL6 and IL17 in peripheral blood of early rheumatoid arthritis shows a weak correlation with disease activity which could not be an ideal biomarker for disease activity in comparison to synovial level of these cytokines.

Disclosure of Interest : H.

Abozaid : None Declared, D.

Jayaraj : None Declared, N Gullick : None Declared, H.

Evans : None Declared, D.

Scott : None Declared, E.

Choy Grant / Research support from : Abbot's laboratories, Chugai Pharma, MSD, Pfizer, Roche and UCB, Consultant for : Abbots laboratories.