Cure8 regulatory brief
The project investigates how TNFR1 and TNFR2 differently control epithelial repair in the colon—mechanisms that may explain why many patients on anti‑TNF biologics do not achieve lasting mucosal healing and could point to new therapeutic targets.
IBD researchers, translational scientists, gastroenterology clinicians, and patients interested in the biology of anti‑TNF response and mucosal healing
This is a project record describing funded preclinical and translational studies rather than clinical trial results. The team will study mesenchymal and fibroblast populations that support crypt epithelial renewal, focusing on TNFR1 signaling in PDGFRA+ cells and on testing TNFR2 activation as a potential pro‑repair therapy.
Methods include novel reporter mice, human colonoids (including samples from anti‑TNF responders and nonresponders), and transcriptional profiling to define repair-associated cell populations. These studies could point to new therapeutic strategies (for example, selective TNFR2 agonism) but do not report patient outcomes yet.
Findings will be foundational and aimed at enabling future therapeutic development and precision approaches to anti‑TNF nonresponse.
NIH Reporter project-record describing funded preclinical and translational work (mouse models, reporter mice, human colonoids, transcriptional profiling). This is not a clinical trial or peer‑reviewed study report; no patient outcome data are presented.
Review the original publication for the complete reporting, methods, and context.
Funding disclosed by the source: National Institute of Diabetes and Digestive and Kidney Diseases - R01DK148982 - $827,905
This Cure8 brief is based on source text from the linked article. Cure8 is informational only and is not a substitute for professional medical advice, diagnosis, or treatment.
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