Abstract

The objective of this study was to identify the key changed subtype of T helper cells (Th cells) and their cytokines in pristane-induced arthritis (PIA) in rats. The severity of arthritis was evaluated by body weight, clinical score, the perimeter of ankle and mid-paw and histological assessment of ankle joints. Cytokines of Th1, Th2 and Th17 were determined in the spleen and inguinal lymph nodes at 28 days after pristane injection by real-time qPCR. The mRNA levels of IL-22 receptors, IL-22R1 and IL-22BP, in the spleen were quantified by real-time qPCR. Additionally, IL-22 expression in synovial membrane was detected by Western blotting, and serum IL-22 concentration was determined by ELISA. Correlation between IL-22 concentration and clinical score was analyzed. By screening the cytokines of Th1, Th2 and Th17 expression profile, we found that the mRNA levels of Th17 cytokines were significantly increased in PIA rats. Particularly, a significant increase in the protein expression of IL-22 was determined in synovial membrane and serum from PIA rats, and correlated with clinical score. We conclude that IL-22 expression level was increased and correlated with disease severity, which indicated that IL-22 may play an important role in development of PIA, and was helpful to explorer the pathogenesis of rheumatoid arthritis.

Highlights

  • Rheumatoid arthritis (RA) is a common chronic autoimmune inflammatory disorder, which is associated with progressive disability, systemic complications, early death, and socioeconomic costs [1]

  • The signs of pristane-induced arthritis (PIA) rat model were evaluated in various aspects, including body weight, clinical score, perimeters of ankle and mid-paw, and pathological changes

  • In the PIA group, the body weight of rats was reduced at 16 days, and a significant reduction was observed after 20 days (Fig 1A)

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Summary

Introduction

Rheumatoid arthritis (RA) is a common chronic autoimmune inflammatory disorder, which is associated with progressive disability, systemic complications, early death, and socioeconomic costs [1]. RA can cause cartilage and bone damage as well as joint functional disability. The cause of RA is not fully known, both adaptive and innate autoimmune processes play important roles in the disease pathogenesis [2, 3]. Through the polarization of naive T cells and induction of autoreactive B cells, the innate immune response could further enhance. Th17 cytokines and PIA role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

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