ArticleJournal of gastroenterology2015
Anti-TNF-alpha loss of response is associated with a decreased percentage of FoxP3+ T cells and a variant NOD2 genotype in patients with Crohn's disease.
Article in Journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.
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Who cites it
11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.
- Pharmacogenetics in Response to Biological Agents in Inflammatory Bowel Disease: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Pooled it
- Gene, genetics and genetic medicines in gastroenterology: Current status and its future.World journal of gastroenterology · 2026Review
- Molecular Insight into the Role of HLA Genotypes in Immunogenicity and Secondary Refractoriness to Anti-TNF Therapy in IBD Patients.International journal of molecular sciences · 2025Review
- Genetic factors that predict response and failure of biologic therapy in inflammatory bowel disease.World journal of experimental medicine · 2025Review
- Pharmacogenomics of TNF inhibitors.Frontiers in immunology · 2025Review
- Peripheral blood regulatory T cells and disease activity, quality of life, and outcomes in children with juvenile idiopathic arthritis.Pediatric rheumatology online journal · 2024Article
- Article
- Predictors and Early Markers of Response to Biological Therapies in Inflammatory Bowel Diseases.Journal of clinical medicine · 2021Review
- The roles and functions of Paneth cells in Crohn's disease: A critical review.Cell proliferation · 2021Review
- Bacterial Translocation as Inflammatory Driver in Crohn's Disease.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAnti-TNF-α therapies interact with the tolerogenic response in patients with Crohn's disease, modulating inflammation. However, drug levels and the genetic background may affect this interaction.
methodsPatients with Crohn's disease in remission on biologic monotherapy were enrolled in this study. FoxP3+ lymphocytes, NOD2 genotype, serum cytokine, anti-TNF-α levels, and anti-drug antibodies were evaluated. Regulatory T cell response to infliximab was evaluated in vitro.
resultsFifty-seven patients were included. Thirty-nine patients (68.4%) were receiving non-intensified biologic therapy whereas 18 patients (31.6%) were under an intensified biologic schedule due to loss of response. Eleven intensified patients (61.1%) showed a variant NOD2 genotype vs 9 on non-intensified biologics (23%, p < 0.01). Percentage of FoxP3+ T cells and serum free anti-TNF-α levels were significantly higher in patients with a wild-type vs variant NOD2 genotype, either under non-intensified or intensified schedule. Increasing amounts of infliximab significantly increased the expression of FoxP3+ T cells and anti-TNF-α levels in the supernatant from wild-type NOD2 patients cultured cells whereas the induction of FoxP3+ T cells and anti-TNF-α levels in the supernatant from variant NOD2 patients cultured cells were significantly lower. TNF-α and IL-10 showed a correlation with the FoxP3+ T cell population percentage and serum levels of anti-TNF-α, irrespective of NOD2 genotype. Eight variant NOD2 patients (66.6%) vs 4 wild-type NOD2 patients (8.8%) showed a perianal phenotype (p = 0.01). A significant reduction of the percentage of FoxP3+ T cells and serum levels of anti-TNF-α was observed in patients with the associated perianal disease.
conclusionAnti-TNF-α loss of response is associated with a decreased percentage of FoxP3+ T cells and a variant NOD2 genotype in patients with CD.
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