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. 2024 Apr 20;51(1):545.
doi: 10.1007/s11033-024-09525-2.

Tumor necrosis factor alpha induced protein 3, interleukin 10, tumor necrosis factor alpha, and interleukin 17 F genes polymorphisms in Algerian patients with rheumatoid arthritis

Affiliations

Tumor necrosis factor alpha induced protein 3, interleukin 10, tumor necrosis factor alpha, and interleukin 17 F genes polymorphisms in Algerian patients with rheumatoid arthritis

D Benahmed et al. Mol Biol Rep. .

Abstract

Background: Rheumatoid arthritis (RA) is a systemic autoimmune disease with chronic inflammation. Its pathogenesis involves immunological, genetic, and environmental factors. We investigate the association between Tumor Necrosis Factor α Protein 3 (TNFAIP3), Interleukin 10 (IL10), Tumor Necrosis Factor α (TNF α), and Interleukin 17 F (IL17F) polymorphisms with susceptibility to RA.

Methods and results: 191 patients with RA diagnosed according to the American College of Rheumatology (ACR)/ European League Against Rheumatism (EULAR) classification and 190 healthy subjects were recruited. Rheumatoid factor (RF), anti-citrullinated peptide antibodies (ACPA), and C-reactive protein (CRP) were measured. Genotyping of the polymorphisms was performed by real-time PCR. Analysis of the allelic frequencies of TNFAIP3 showed a positive association OR (95% CI) = 1.46 (1.01-2.09); p = 0.04, but failed to meet the criteria of significance after Bonferroni Correction. The genotypic and allelic distribution of the IL10, IL17F, and TNFα showed no significant difference when comparing the RA group with controls. Furthermore, the genotype codominant model shows a moderate positive association in the presence of ACPA (OR (95% CI) = 2.82 (1.22-6.24); p = 0.01. None of the polymorphisms studied was associated with RF and CRP production.

Conclusion: Our results show that there is a tendency for the AG genotype of IL10-1082 to be associated with the production of ACPA in patients with RA. None of the variants studied were associated with RA susceptibility in Algerians.

Keywords: Autoantibodies; IL10; IL17F; Rheumatoid arthritis; TNFAIP3; TNFα.

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References

    1. Firestein GS, McInnes IB (2017) Immunopathogenesis of rheumatoid arthritis. Immunity. https://doi.org/10.1016/j.immuni.2017.02.006
    1. Shrivastava AK, Singh HV, Raizada A, Singh SK, Pandey A, Singh N, Yadav DS, Sharma H (2015) Inflammatory markers in patients with rheumatoid arthritis. https://doi.org/10.1016/j.aller.2013.11.003 . Allergol immunopathol
    1. Mikhaylenko DS, Nemtsova MV, Bure IV, Kuznetsova EB, Alekseeva EA, Tarasov VV et al (2020) Genetic polymorphisms associated with rheumatoid arthritis development and antirheumatic therapy response. Int J Mol Sci. https://doi.org/10.3390/ijms21144911 - DOI - PubMed - PMC
    1. Hess A, Axmann R, Rech J, Finzel S, Heindl C, Kreitz S et al (2011) Blockade of TNF-α rapidly inhibits pain responses in the central nervous system. Proc Nat Acad Sci. https://doi.org/10.1073/pnas.1011774108 - DOI - PubMed - PMC
    1. Reynolds JM, Angkasekwinai P, Dong C (2010) IL-17 family member cytokines: regulation and function in innate immunity. Cytokine Growth Factor Rev. https://doi.org/10.1016/j.cytogfr.2010.10.002 - DOI - PubMed - PMC

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