Abstract

Immune Complexes and Complement in Serum and Synovial Fluid of Rheumatoid Arthritis PatientsRheumatoid arthritis (RA) is predominantly an intraarticular inflammatory and autoimmune disease that involves different autoantibodies and effector mechanisms. The aim of the study was to determine the utility of Circulating Immune Complexes (CIC) and complement components (C3c, C4) as possible markers for the disease activity in laboratory diagnostics. In a cross-section study 59 patients, according to the clinical criteria, were categorized into two groups: group with moderate (MA, n=24), and group with severe activity (SA, n=35) of RA. The concentration of CIC, C3c and C4 in sera (S) and synovial fluids (SF) was examined by an immunonephelometric method in both groups and compared with values in the control group (n=15) of patients with lesions of the menisci. Obtained results showed that there was no statistical significance in the values of C3c and C4, in both biological fluids, among all tested groups. Significant differences were found in the levels of CIC in both fluids, while testing the parameters (× ± SD, IU/mL) in the sera of groups with SA and MA of RA: 7.43 ± 13.40; 3.01 ± 2.92 (p<0.05) and SF: 13.47 ± 21.1, 5.33 ± 7.53 (p<0.001), respectively. These differences were higher between the group with SA and CG. Results for the concentrations of CIC were significantly higher in SF compared to sera: in the RA group with SA by 77% and group with MA by about 82%. These data could provide a confirmation of the hypothesis about local, intraarticular autoantibodies and subsequent CIC production. It can be concluded that the examination of CIC concentration in serum, and where it is possible in SF, is a useful marker of disease activity in RA patients, in contrast to the tested components of the complement. This statement does not exclude their consumption within immune effector mechanisms, but elicits the possibility that lower molecular fragments (C3d, C4d), as well as the novel activation products, could be better disease activity markers in RA patients.

Highlights

  • Rheumatoid arthritis (RA) is a chronic autoimmune synovitis affecting about 1.0% of the world’s population [1], but the mechanisms underlying the initiation and progression of RA are not yet completely understood

  • In the groups with moderate and severe RA activity, the average values of Circulating Immune Complexes (CIC) were more than 80 percent higher in synovial fluids (SF), which is statistically highly significant (p

  • The comparison of complement components and CIC concentration in the tested biological fluids in two different RA activity groups and the control group is presented in Tables II –IV

Read more

Summary

Introduction

Rheumatoid arthritis (RA) is a chronic autoimmune synovitis affecting about 1.0% of the world’s population [1], but the mechanisms underlying the initiation and progression of RA are not yet completely understood. Apart from rheumatoid factor (RF-IgM) and different RF isotypes [6,7,8], other autoantibodies have been added to the growing list of autoantigens such as: filaggrin [10], Sa [11, 12], calpastin [13], RA33 [14], collagen type II [15] and a number of citrullinated proteins [16,17,18]. Due to their ability to form ICs, they may promote complement activation. RA is a classic example of a multifactorial disease in which a combination of genetic and environmental factors contributes to the disease progression

Objectives
Methods
Results
Discussion
Conclusion

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

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.