The pathophysiology of inflammatory bowel diseases has been studied in three different mouse models of experimental colitis, DSS, TNBS and the CD45RB transfer colitis (te Velde et al, 2006). Following this, a critical appraisal of the current practice in murine TNBS-induced colitis has been written (te Velde et al, 2006). Also, in a follow up study the role of overlapping gene expression in the mouse models is studied in human inflammatory bowel diseases (te Velde et al, submitted). In an other study the balance between inhibitory signals (provided by the C-type lectins (CLRs) and activation signals (provided by the Toll-like receptors (TLRs) and NACHT-LRR (NLRs) in relation to IBD is studied. Mutations in one or more of the involved pattern recognition receptors (PRRs) might disturb this precious balance. This study has resulted in a grant (MLDS) in which we will determine if single nucleotide polymorphisms (SNPs) in genes clustered in the IBD2 and IBD6 susceptibility loci for IBD (especially C-type lectins) and NACHT-LRR members (especially NALP-3) play a role in the pathogenesis of inflammatory bowel diseases. Finally apoptose in relation to IBD has been studied (Verstege et
al, 2006 and van den Brande et al, 2007).

Theme: Immunity and Infections
Effective start/end date01/01/2007 → …

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