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Investigating the immunomodulatory effects of quercetin on cytokine signalling pathways in rheumatoid arthritis and type 1 diabetes

A. Saad, A. Dalhat, B. Ali

International journal of science research and technology, 2026

6 participants

Abstract

Autoimmune diseases such as rheumatoid arthritis (RA) and type 1 diabetes (T1D) are characterised by persistent dysregulation of immune signalling pathways driven by aberrant cytokine activity and impaired negative-feedback mechanisms. Central mediators of this pathogenic network include interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), signal transducer and activator of transcription 3 (STAT3), and suppressor of cytokine signalling 3 (SOCS3). These four targets were prioritised because they constitute the core IL-6/TNF-α–JAK/STAT3–SOCS3 regulatory axis that remains incompletely characterised at the protein and transcript level in human autoimmune peripheral blood mononuclear cells (PBMCs) following flavonoid intervention. This study evaluates the molecular impact of quercetin, a dietary flavonoid with documented antioxidant and immunomodulatory properties, on these cytokine-signalling pathways in patients with RA and T1D. Ten participants (RA, n = 6; T1D, n = 4) enrolled in a prospective, single-arm, open-label pilot trial orally self-administered 500 mg quercetin daily for 30 days. Peripheral blood mononuclear cells (PBMCs) and serum samples were collected at baseline (Day 0) and post-treatment (Day 30) and analysed by quantitative reverse-transcription PCR (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and Western blot. A ≥ 1.5-fold change from baseline was used to define a molecular responder. Paired Wilcoxon signed-rank tests were applied; effect sizes…

How strong is the evidence?

Evidence Hub reads this as a randomized trial, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence. Reported size: 6 participants or records.

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