Abstract

Controversial results concerning the association between a polymorphism rs6822844 in the interleukin (IL) 21 (IL-21) gene and rheumatoid arthritis (RA) have existed. A meta-analysis to confirm above relationships is necessary to be performed immediately. We conducted a search in the PubMed database, covering all papers published up to 20 October 2018. Overall, six case–control studies with 3244 cases and 3431 healthy controls were included. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of this association. Publication bias was assessed with both Egger’s and Begg’s tests. After calculation, we found that IL-21 rs6822844 polymorphism could decrease RA risk in overall genetic models (allelic contrast: OR = 0.77, 95% CI = 0.62–0.97, P=0.024; TG versus GG: OR = 0.68, 95% CI = 0.50–0.92, P=0.013, and dominant genetic model: OR = 0.72, 95% CI = 0.55–0.94, P=0.016). Similarly, stratified analysis by race, source of control, significantly decreased association was found in Asians, Caucasians and hospital-based (HB) control source. Finally, in the subgroup analysis of rheumatoid factor (RF) and anti-citrullinated protein antibody (ACPA) status, poorly decreased relationship was detected between IL-21 rs6822844 polymorphism and RF negative and ACPA positive RA risk, respectively. No obvious evidence of publication bias was detected in overall analysis. In summary, our study indicated that IL-21 rs6822844 polymorphism was significantly associated with decreased RA susceptibility.

Highlights

  • Received: 16 January 2019Revised: 01 June 2019Accepted: July 2019Accepted Manuscript Online: July 2019Version of Record published: 15 August 2019Rheumatoid arthritis (RA) is a systemic, inflammatory autoimmune disorder with numerous manifestations caused due to intricate chain of events [1]

  • Characteristics of studies of IL-21 rs6822844 polymorphism are summarized in Tables 1 and 2

  • rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic persistent synovial joint inflammation resulting in bony erosion, cartilage loss, and often systemic disorders, such as subcutaneous rheumatoid nodules, secondary Sjogren’s syndrome, interstitial lung disease, and systemic vasculitis [28,29]

Read more

Summary

Introduction

Received: 16 January 2019Revised: 01 June 2019Accepted: July 2019Accepted Manuscript Online: July 2019Version of Record published: 15 August 2019Rheumatoid arthritis (RA) is a systemic, inflammatory autoimmune disorder with numerous manifestations caused due to intricate chain of events [1]. Cells of the leukocyte lineage such as: monocytes-macrophages, neutrophils, mastocytes, and subsets of T and B cells majorly contribute to the pathogenesis of RA by secreting various cytokines and chemokines [2]. Interleukin (IL) 21 (IL-21), a dual role cytokine discovered during the year 2000 shares similar homology with IL-2 family of cytokines (IL-2, IL-4, and IL-15) [3]. IL-21 interacts with γ chain (γc) of IL-21 receptor (IL-21R) expressed in various immune cells of the leukocyte lineage. IL-21 is predominantly secreted by T helper 17 (Th17) follicular T helper (Tfh) and natural killer T (NKT) cells [4]. IL-21 has been found to be a key player in RA pathogenesis and progression [5,6,7].

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call