Immune Interaction between Interleukin-22 and Interleukin-26 and Its Relationship with Rheumatoid Arthritis Disease Activity
DOI:
https://doi.org/10.61704/pr.634الكلمات المفتاحية:
Rheumatoid Arthritis، IL-22، IL-26، Cytokines، DAS28، Inflammatoryالملخص
Abstract
Rheumatoid arthritis (RA) is a chronic autoimmune condition in which persistent synovial inflammation gradually alters joint structure and function. Increasing attention has been directed toward Th17-related cytokines—particularly interleukin-22 (IL-22) and interleukin-26 (IL-26) because of their potential contribution to sustained inflammation and disease progression in RA. This study aimed to quantify serum IL-22 and IL-26 levels in patients with RA and to determine their relationship with disease activity assessed using the DAS28 score. A case-control study was conducted involving 50 RA patients and 35 age- and sex-matched healthy individuals. Serum IL-22 and IL-26 concentrations were measured using ELISA, while disease activity was assessed using DAS28. Appropriate statistical tests were applied to compare groups and examine correlations. Patients with RA exhibited markedly elevated IL-22 levels (178.5 ± 61.3 pg/mL) compared with controls (96.4 ± 39.7 pg/mL, p < 0.001). Likewise, IL-26 concentrations were significantly higher in RA patients (142.7 ± 55.9 pg/mL) than in controls (71.8 ± 28.6 pg/mL, p < 0.001). Serum IL-22 showed a moderate positive correlation with DAS28 (r = 0.49, p < 0.001), and IL-26 demonstrated a slightly stronger association (r = 0.53, p < 0.001). A notable correlation was also observed between IL-22 and IL-26 themselves (r = 0.57, p < 0.001). The clear elevation of IL-22 and IL-26 in RA patients, along with their strong correlations with disease activity, supports their potential role as useful supportive biomarkers for monitoring inflammatory burden and evaluating disease progression.
المراجع
Al-tai, T. H. H. (2024). Serum IL-22 in patients with rheumatoid arthritis. African Journal of Biomedical Research, 27(3), 2487–2491. https://doi.org/10.53555/AJBR.v27i3.5701
Biedermann, T., Skabytska, Y., Kaesler, S., & Volz, T. (2015). Regulation of T cell immunity in atopic dermatitis by microbes: The yin and yang of cutaneous inflammation. Frontiers in Immunology, 6, Article 353. https://doi.org/10.3389/fimmu.2015.00353
Choy, E. H. S., & Panayi, G. S. (2001). Cytokine pathways and joint inflammation in rheumatoid arthritis. The New England Journal of Medicine, 344(12), 907–916. https://doi.org/10.1056/NEJM200103223441207
Corvaisier, M., Delneste, Y., Jeanvoine, H., Preisser, L., Blanchard, S., Garo, E., Hoppe, E., Barré, B., Audran, M., Bouvard, B., Saint-André, J.-P., & Jeannin, P. (2012). IL-26 is overexpressed in rheumatoid arthritis and induces proinflammatory cytokine production and Th17 cell generation. PLOS Biology, 10(9), Article e1001395. https://doi.org/10.1371/journal.pbio.1001395
Cross, M., Smith, E., Hoy, D., Carmona, L., Wolfe, F., Vos, T., Williams, B., Gabriel, S., Lassere, M., Johns, N., Buchbinder, R., Woolf, A., & March, L. (2014). The global burden of rheumatoid arthritis: Estimates from the Global Burden of Disease 2010 study. Annals of the Rheumatic Diseases, 73(7), 1316–1322. https://doi.org/10.1136/annrheumdis-2013-204627
Chen, H., Schürch, C. M., Noble, K., Kim, K., Krutzik, P. O., O’Donnell, E., Vander Tuig, J., Nolan, G. P., & McIlwain, D. R. (2020). Functional comparison of PBMCs isolated by Cell Preparation Tubes (CPT) vs. Lymphoprep Tubes. BMC Immunology, 21, Article 15. https://doi.org/10.1186/s12865-020-00345-0
Firestein, G. S., & McInnes, I. B. (2017). Immunopathogenesis of rheumatoid arthritis. Immunity, 46(2), 183–196. https://doi.org/10.1016/j.immuni.2017.02.006
Gaffen, S. L., Jain, R., Garg, A. V., & Cua, D. J. (2014). The IL-23–IL-17 immune axis: From mechanisms to therapeutic testing. Nature Reviews Immunology, 14(9), 585–600. https://doi.org/10.1038/nri3707
Ikeuchi, H., Kuroiwa, T., Hiramatsu, N., Kaneko, Y., Hiromura, K., Ueki, K., & Nojima, Y. (2005). Expression of interleukin-22 in rheumatoid arthritis: Potential role as a proinflammatory cytokine. Arthritis & Rheumatism, 52(4), 1037–1046. https://doi.org/10.1002/art.20965
Kondo, N., Kuroda, T., & Kobayashi, D. (2021). Cytokine networks in the pathogenesis of rheumatoid arthritis. International Journal of Molecular Sciences, 22(20), Article 10922. https://doi.org/10.3390/ijms222010922
Lubberts, E. (2015). The IL-23–IL-17 axis in inflammatory arthritis. Nature Reviews Rheumatology, 11(7), 415–429. https://doi.org/10.1038/nrrheum.2015.53
Lundström, E., Källberg, H., Alfredsson, L., Klareskog, L., & Padyukov, L. (2009). Gene–environment interaction between the DRB1 shared epitope and smoking in the risk of anti–citrullinated protein antibody–positive rheumatoid arthritis: All alleles are important. Arthritis & Rheumatism, 60(6), 1597–1603. https://doi.org/10.1002/art.24572
McInnes, I. B., & Schett, G. (2011). The pathogenesis of rheumatoid arthritis. The New England Journal of Medicine, 365(23), 2205–2219. https://doi.org/10.1056/NEJMra1004965
Mitra, A., Raychaudhuri, S. K., & Raychaudhuri, S. P. (2012). Functional role of IL-22 in psoriatic arthritis. Arthritis Research & Therapy, 14(2), Article R65. https://doi.org/10.1186/ar3781
Ma, W.-T., Gao, F., Gu, K., & Chen, D.-K. (2019). The role of monocytes and macrophages in autoimmune diseases: A comprehensive review. Frontiers in Immunology, 10, Article 1140. https://doi.org/10.3389/fimmu.2019.01140
Nadi, E., Arjipour, M., Sharifi, S., & Zamani, A. (2014). Assay of IL-22 and IL-25 in serum, whole blood, and peripheral blood mononuclear cell cultures of patients with severe asthma. Allergologia et Immunopathologia, 42(5), 402–406. https://doi.org/10.1016/j.aller.2013.03.006
Ouyang, W., Kolls, J. K., & Zheng, Y. (2008). The biological functions of T helper 17 cell effector cytokines in inflammation. Immunity, 28(4), 454–467. https://doi.org/10.1016/j.immuni.2008.03.004
Pan, H.-F., Li, X.-P., Zheng, S. G., & Ye, D.-Q. (2013). Emerging role of interleukin-22 in autoimmune diseases. Cytokine & Growth Factor Reviews, 24(1), 51–57. https://doi.org/10.1016/j.cytogfr.2012.07.002
Roeleveld, D. M., & Koenders, M. I. (2015). The role of the Th17 cytokines IL-17 and IL-22 in rheumatoid arthritis pathogenesis and developments in cytokine immunotherapy. Cytokine, 74(1), 101–107. https://doi.org/10.1016/j.cyto.2014.10.006
Smolen, J. S., Aletaha, D., & McInnes, I. B. (2016). Rheumatoid arthritis. The Lancet, 388(10055), 2023–2038. https://doi.org/10.1016/S0140-6736(16)30173-8
Sonnenberg, G. F., Fouser, L. A., & Artis, D. (2011). Border patrol: Regulation of immunity, inflammation and tissue homeostasis at barrier surfaces by IL-22. Nature Immunology, 12(5), 383–390. https://doi.org/10.1038/ni.2025
Tanaka, T., Narazaki, M., & Kishimoto, T. (2014). IL-6 in inflammation, immunity, and disease. Cold Spring Harbor Perspectives in Biology, 6(10), Article a016295. https://doi.org/10.1101/cshperspect.a016295
Too, C. L., Yahya, A., Murad, S., Dhaliwal, J. S., Larsson, P. T., Muhamad, N. A., Abdullah, N. A., Mustafa, A. N., Klareskog, L., Alfredsson, L., Padyukov, L., Bengtsson, C., & MyEIRA Study Group. (2012). Smoking interacts with HLA-DRB1 shared epitope in the development of anti-citrullinated protein antibody-positive rheumatoid arthritis: Results from the Malaysian Epidemiological Investigation of Rheumatoid Arthritis (MyEIRA). Arthritis Research & Therapy, 14(2), Article R89. https://doi.org/10.1186/ar3813
Wang, Y.-H., Peng, Y.-J., Liu, F.-C., Lin, G.-J., Huang, S.-H., Sytwu, H.-K., & Cheng, C.-P. (2023). Interleukin 26 induces macrophage IL-9 expression in rheumatoid arthritis. International Journal of Molecular Sciences, 24(8), Article 7526. https://doi.org/10.3390/ijms24087526
Xie, Q., Huang, C., & Li, J. (2015). Interleukin-22 and rheumatoid arthritis: Emerging role in pathogenesis and therapy. Autoimmunity, 48(2), 69–72. https://doi.org/10.3109/08916934.2014.959165
التنزيلات
منشور
كيفية الاقتباس
إصدار
القسم
الرخصة
الحقوق الفكرية (c) 2026 Ali M. Abd-Alameer

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