Cytokine-Mediated Intestinal and Systemic Immune Dysregulation in Inflammatory Bowel Disease, Celiac Disease, and Autoimmune Hepatitis: A Systematic Review and Meta-Analysis of Biomolecular Mechanisms and Therapies
Keywords:
Autoimmune, Celiac Disease, Crohn Disease, Cytokines, Th17 Cells, hepatitis, IL-17, InterleukinsAbstract
Background: Cytokine-mediated immune dysregulation is important in the pathogenesis of autoimmune and inflammatory diseases, such as inflammatory bowel disease, celiac disease, and autoimmune hepatitis. This paper set out to undertake a systematic review of cytokine-mediated immune mechanisms, especially the IL-17, in these conditions.
Methods: PRISMA 2020 was used in this systematic review. Up to March 2026, the electronic databases such as PubMed, Scopus, Web of Science, and Google Scholar were searched. Articles that reported cytokine levels or immune biomarkers in patients with inflammatory bowel disease, celiac disease, or autoimmune hepatitis versus those without any disease or animal studies, reviews, case reports, and studies of which quantitative cytokine levels were not measured were excluded. The synthesis of data was done qualitatively and quantitatively and meta-analysis was done on the synthesized data using random-effects model to estimate pooled standardized mean differences.
Results: 443 articles were found, out of which 15 articles were eligible to include in the systematic review, and a subset of them was added to the meta-analysis. The combined findings showed very high levels of circulating IL-17 in celiac disease patients in comparison with healthy controls, but no significant differences were found between Crohn disease patients and autoimmune hepatitis patients. In a number of the observational studies, the risk of bias was moderate and was assessed.
Conclusion: IL-17–mediated immune dysregulation is significantly elevated in celiac disease but not consistently in Crohn’s disease or autoimmune hepatitis, while IL-23 significantly increased in autoimmune hepatitis. These findings highlight disease-specific roles of IL-23/Th17-related pathways and the need for larger, standardized studies.
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