FCGR2A and inflammatory bowel disease: Secondary considerations regarding this differential association arise from the inflammatory networks contributing to CD and UC pathogenesis.64 While the IL-23-Th17 axis is central to both IBD subclasses, lamina propria cells isolated from CD and UC patients produce excessive levels of IFNγ and IL-13, respectively.64,65 In turn, this may impact the consequences of FcγR signalling by intestinal immune cell subsets.