Tumor Necrosis Factor-Like Ligand 1A/Death Receptor 3 Signaling Regulates the Generation of Pathogenic T Helper 9 Cells in Experimental Crohn’s Disease

We demonstrate that the functional DR3 receptor is essential for Th9 cell pathogenicity, revealing a new mechanism by which TL1A/DR3 signaling drives experimental CD-like ileitis. The TL1A/DR3/Th9 proinflammatory pathway may offer a novel therapeutic target for patients with CD.