Celiac disease is an immune-mediated enteropathy triggered by gluten ingestion. The effect of very small gluten exposures remains uncertain, contributing to international variations in food-labelling standards. Interleukin-2 rises rapidly after gluten ingestion serving as a biomarker of immune activation. We aimed to identify the lowest gluten dose that elicits a measurable interleukin-2 response and accompanying symptoms in treated celiac disease.

Immune-mediated inflammatory diseases are undergoing a paradigm shift from treatment of established pathology toward prevention in at-risk individuals. Celiac disease (CeD), driven by an aberrant immune response to dietary gluten in genetically predisposed subjects, represents an ideal model to investigate the transition from tolerance to autoimmunity. Within this framework, potential celiac disease (PCD)-defined by CeD-specific autoantibodies in the absence of villous atrophy-has emerged as a clinically relevant condition whose natural history, heterogeneity, and predictors of progression are increasingly understood. Immunological studies reveal that PCD is characterized by a blunted Th1 response, preserved regulatory pathways, reduced epithelial stress signalling, and incomplete licensing of cytotoxic IELs, preventing tissue destruction. This distinct immunological landscape makes PCD a unique window to dissect mechanisms underlying loss of tolerance and to explore preventive strategies. Only a subset of PCD individuals progress to active CeD, with the highest risk concentrated in the first years following seroconversion, while other even stop producing autoantibodies despite consuming gluten. Clinical management remains controversial, but current guidelines discourage routine gluten-free diet (GFD) in asymptomatic PCD both in children and in adults. In conclusion, PCD represents a heterogeneous but highly informative condition positioned at the crossroads between genetic susceptibility and mucosal damage. The identification of reliable progression markers and the development of targeted preventive interventions could transform CeD management and contribute broadly to the understanding and prevention of organ-specific autoimmunity.

Postoperative biliary and vascular complications (including stenosis, thrombosis, and occlusion) after liver transplantation (LT) can impair graft function, increase reoperation needs, and elevate patient mortality, significantly affecting long-term survival. The clinical reference standards magnetic resonance cholangiopancreatography (MRCP) for biliary complications is expensive and time-consuming, while computed tomography angiography (CTA) for vascular complication involves ionizing radiation and allergic reaction to contrast agents, limiting their repeated use during follow-up. Ultrasound viscoelastic imaging (UVI), an affordable, non-invasive technique, could be an effective alternative. This study aims to assess the clinical value of UVI in auxiliary diagnosis of biliary and vascular complications post-LT.