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CD is a chronic immune-mediated enteropathy triggered by gluten ingestion in genetically predisposed subjects (1). In CD the immunology response to gluten causes histology abnormalities of the small bowel mucosa eventually leading to villous atrophy and secondary vitamins, and nutrients malabsorption (1,2). In affected individuals, recent evidence suggests that gluten evokes a signaling cascade which triggers an inflammatory reaction with cytokine release resulting in additional intestinal mucosal barrier dysfunction for damage of tight junction proteins (e.g., Zonulin), so called “leaky gut” syndrome (2). The increased intestinal permeability allows gluten peptides to reach the lamina propria via either a para-cellular or intracellular route thus aggravating inflammation with systemic complications (2,3). A recent meta-analysis provided evidence of increasing incidence of celiac disease in the western world mostly in the pediatric population and in females (4). In the 21st century, the pooled female incidence of CD was 17.4 new cases per 100,000 person-years, compared with 7.8 in males. When considering the pediatric incidence, it was found to be 21.3 per 100,000 person-years compared to 12.9 in adults (4). Notwithstanding this data, CD recognition can be challenging with functional gastrointestinal disorders frequently misdiagnosed instead (1,5). Moreover, CD shows a complex clinical scenario from life-threatening manifestations of severe malabsorption to minimally symptomatic or even non-symptomatic presentations. The clinical picture of adult CD is dominated by gastrointestinal symptoms: diarrhea, bloating, flatulence, abdominal pain, while systemic manifestations (e.g., weight loss, fatigue) are less common. However, extra intestinal manifestations might include: dermatological symptoms (dermatitis herpetiformis), neurologic symptoms (seizures, motor weakness, paresthesia and ataxia) and hormonal imbalance of both reproductive and infertility ages (1). Current guidelines recommend plasma testing of antitransglutaminase antibody to screen for CD in both adults and children when symptoms are suggestive and/or at high genetic risk as first degree relative of CD patients (1). However, duodenal biopsies are still mandatory to confirm the diagnosis in adults (1). Main histopathologic characteristics of CD include modifications of the small intestine mucosa: deteriorated villi with a decreased villousto-crypt ratio (VHCD), hyperplastic crypts, with increased number of intraepithelial lymphocytes (IEL) per unit length of absorptive epithelium (normal IEL to epithelial cell ratio, 1:10) (2). Architectural changes in the mucosa can be precisely quantified and analyzed using the VHCD. The normal VHCD is considered between 4–5:1. A lower Editorial Commentary

Anti-IL-15 monoclonal antibody for the treatment of coeliac disease: the light at the end of the gluten free diet tunnel?