Introduction: Inflammatory bowel diseases (IBD), encompassing Crohn's disease (CD) and ulcerative colitis (UC), present ongoing challenges despite advances in pathophysiological understanding and therapeutic options. Current therapies often fail to achieve sustained remission, necessitating exploration of novel treatment targets.
Areas Covered: This review explores the role of Tumor Necrosis Factor-like cytokine 1A (TL1A) and its receptor DR3 in IBD pathogenesis, detailing their involvement in mucosal homeostasis and immune modulation.
WNT3A is an intestinal ligand triggering the Wnt/β-catenin (Wnt) pathway, which can be enhanced by R-spondin 1 (RSPO1) through the RSPO1-LGR axis or antagonized by the adenomatous polyposis coli (APC) protein supporting β-catenin-degradation. Wnt interplays with several pathways including PI3K/mTOR (mTOR). In this study, we evaluated the influence of WNT3A-commercial and home-made culture media and RSPO1 protein on the Wnt and mTOR interplay in non-APC and APC-mutated intestinal patient-derived organoids (PDOs).
View Article and Find Full Text PDFObjectives: Chagas disease (CD), or American trypanosomiasis, is a parasitic disease caused by Trypanosoma cruzi, primarily transmitted by triatomine bugs. Increased travels and migrations introduced CD to non-endemic regions, including Europe. In Italy, the disease has raised public attention mainly in northern regions, where Latin American migrant population is larger.
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