Intestinal homeostasis relies on the symbiotic nature of host-microbe interactions. Loss of this symbiosis can trigger immune dysregulation and is considered to shape the susceptibility to inflammatory bowel diseases (IBD), a complex trait influenced by genetic predisposition and environmental cues. The rare X-linked lymphoproliferative syndrome type 2 (XLP2) is caused by mutations in XIAP and is often linked to IBD, but the role of XIAP in IBD is largely unexplored. By using genetic mouse models, this thesis elucidates how XIAP restricts mucosal inflammation driven by TNF.
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Intestinal homeostasis relies on the symbiotic nature of host-microbe interactions. Loss of this symbiosis can trigger immune dysregulation and is considered to shape the susceptibility to inflammatory bowel diseases (IBD), a complex trait influenced by genetic predisposition and environmental cues. The rare X-linked lymphoproliferative syndrome type 2 (XLP2) is caused by mutations in XIAP and is often linked to IBD, but the role of XIAP in IBD is largely unexplored. By using genetic mouse model...
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