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Significance This study describes a role for tumor necrosis factor ligand superfamily member 15 (TNFSF15), a molecule being considered for therapy in inflammatory diseases. We identify that death receptor 3 (DR3) is clearly expressed on human macrophages and define a new role for TNFSF15:DR3 signaling in mediating innate immune outcomes in human myeloid-derived cells, as well as mechanisms mediating these outcomes. We further define the disease-relevant, functional consequences of polymorphisms in theTNFSF15 region, one of the 163 inflammatory bowel disease risk loci. To our knowledge, our studies highlight a previously unknown mechanism through which TNFSF15:DR3 can contribute to intestinal inflammation, namely by enhancing signaling and cytokine secretion upon stimulation of a broad range of pattern-recognition-receptors, mycobacterial components, and live bacteria.

A TNFSF15 disease-risk polymorphism increases pattern-recognition receptor-induced signaling through caspase-8–induced IL-1