Cure8 research brief
If validated, IGFBP5 or its downstream pathway could help predict who will not respond to anti-TNF therapy and point to new targets to overcome resistance.
Researchers studying IBD treatment resistance and biomarkers; clinicians interested in mechanisms of anti-TNF failure and future predictive tests; translational scientists exploring fibroblast-mediated inflammation.
The paper integrates bulk transcriptomics, single-cell RNA-seq, and spatial transcriptomics from clinical cohorts and validates findings in independent samples and in vitro experiments.
IGFBP5 was enriched in fibroblasts from patients who did not respond to infliximab and linked to an immune-activated microenvironment, including increased signaling to monocytes, endothelial cells, and T cells via VEGF, MIF, and WNT pathways.
The authors report functional data suggesting IGFBP5 activates a VEGFR2/EGR1 signaling axis and increases secretion of inflammatory mediators (IL-6, CXCL12, CCL2) in vitro, supporting a mechanistic role in anti-TNF resistance.
This is an abstract-level summary of a Frontiers in Immunology article (structured-content depth: abstract); Cure8 has not independently verified the full study beyond the supplied article text.
This classification is based on the article abstract and supplied full-text extraction. Findings are preclinical/observational and would need further validation in prospective clinical studies before changing clinical care.
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