ArticleFrontiers in immunology2026
Case Report: Dupilumab-associated ulcerative colitis: elucidating the pathomechanistic link between Th2 blockade and Th17 polarized intestinal inflammation.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Hypersensitivity Reactions to Biologics: Advances in Diagnosis and Management.Current allergy and asthma reports · 2026Review
- Neuroimmune Interactions in Inflammatory Skin and Intestinal Diseases.Journal of inflammation research · 2026Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While dupilumab is highly effective in managing moderate-to-severe atopic dermatitis (AD) through targeted IL-4/IL-13 receptor antagonism, its broader immunomodulatory effects warrant careful clinical scrutiny. We report the case of a 63-year-old male who developed ulcerative colitis (UC) following dupilumab therapy. Although his cutaneous condition improved rapidly, the patient developed acute gastrointestinal distress, including hematochezia and tenesmus, within three months of initiating therapy. Subsequent colonoscopy and histopathological analyses confirmed the diagnosis of UC. Discontinuation of dupilumab was followed by a robust clinical and endoscopic remission. Longitudinal immunohistochemical profiling of the colonic mucosa demonstrated elevated IL-17 and suppressed IL-4 expression during active colitis, which normalized upon clinical recovery. These findings offer hypothesis-generating evidence indicative of a localized Th2-to-Th17 immune shift. Although inherently limited as a single-patient report, this case underscores the critical necessity for multidisciplinary vigilance regarding paradoxical Th17-driven inflammation in patients undergoing IL-4Rα blockade.
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