SEMF-dependent IBD patient heterogeny is also highlighted in the research by Beswick et al. They showed that SEMFs isolated from inflamed intestinal regions of UC patients have a stronger capacity to suppress Th1 cell activity than CD or healthy SEMFs, as they overexpress programmed cell death protein 1 (PD-1), a molecule implicated in the regulation of Th immune responses [32]. This evidence concerns the gene PDCD1 and inflammatory bowel disease.