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Th1/Th17 cytokine signatures correlate with Crohn’s disease activity in a 54‑week cohort of patients treated with adalimumab

Year: 2026

Type: article

Abstract: Crohn's disease (CD) is a chronic inflammatory disorder of the gastrointestinal tract with a relapsing-remitting course. Cytokine dysregulation plays a central role in its pathogenesis, and biological therapies-such as anti‑TNFα agents, vedolizumab, and anti‑IL‑23 monoclonal antibodies-have improved disease control. However, variability in therapeutic response underscores the need for biomarkers to support personalized treatment strategies. A longitudinal study was conducted in 26 patients with clinical‑remission/mild‑activity CD who were treated with adalimumab over 54 weeks. Serum samples were collected at baseline, week 14, and week 54. Eighteen cytokines were quantified using high‑sensitivity Luminex MAP technology. TNFα values were excluded due to drug interference. Clustering and PERMANOVA analyses were used to explore cytokine profiles and their association with disease activity. Four cytokine clusters were identified: Th1‑like, Th2‑like, Th17‑like, and a mixed inflammatory profile including IL‑1β, IL‑2, IL‑12, IL‑21, and IL‑23. Significant reductions in CDAI, C‑reactive protein (CRP), and fibrinogen were observed during treatment. IL‑2, IL‑10, and CCL20 levels increased significantly in patients with active CD (CDAI ≥ 150). Th1 and Th17 signatures were positively correlated with disease activity. Serum assessment of Th1 (IL‑1β, IL‑7) and Th17 (GM‑CSF) signatures generated ROC curves with an AUC of 0.795, compared with CRP (AUC = 0.686) and fibrinogen (AUC = 0.774). Serum cytokine profiling reveals immunological heterogeneity in CD patients treated with adalimumab and may serve as an exploratory biomarker of disease activity and therapeutic response; however, these findings are hypothesis generating and require validation in larger, independent cohorts before clinical applicability can be established.

Source: Biomedicine & Pharmacotherapy

DOI: 10.1016/j.biopha.2026.119508