Yale University has received a USD 2.3 million NIAID P01 program project grant to investigate the immunopathogenesis of celiac disease, with a dual focus on identifying therapeutic targets and developing clinically actionable biomarkers of disease activity — areas where no approved treatments currently exist.
Celiac disease affects roughly 1% of the global population, yet the precise mechanism by which cytotoxic T lymphocytes (CTLs) destroy intestinal epithelial cells remains poorly understood. The central hypothesis driving this consortium is that intraepithelial CTLs recognize gluten-derived peptides presented directly by villous epithelial cells via MHC class I molecules — a mechanistic question with direct implications for drug development. Three integrated projects will address this using technologies not previously applied in celiac disease research, including spatial transcriptomics, pan-expansion microscopy, focused ion beam-scanning electron microscopy, immunopeptidomics, and CITE-seq multiomics. A humanized mouse platform, developed over more than a decade, will enable preclinical therapeutic testing where human tissue access is ethically or logistically constrained.
The grant is led by Jordan S. Pober at Yale School of Medicine, with clinical specimen collection coordinated across four academic medical centers: Yale, Children's Hospital Colorado, Massachusetts General Hospital, and Vanderbilt University Medical Center. The multi-site structure positions the program to integrate tissue-level, blood-based, and systems immunology data with real-world clinical phenotypes. Celiac disease has no approved pharmacotherapy beyond a gluten-free diet, and the absence of validated non-invasive biomarkers of mucosal healing remains a significant gap for both clinical management and trial design.
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