作者: Sonia S. Kupfer , Bana Jabri
DOI: 10.1016/J.GIEC.2012.07.003
关键词:
摘要: Celiac disease is an intestinal inflammatory that triggered by dietary gluten, a protein found in wheat, barley and rye genetically susceptible individuals.1 Descriptions of celiac disease-like phenotype can be traced back to the Greek physician Aretaeus 1st 2nd century AD (reviewed 2). Gluten was identified as culprit Dutch physicians who observed that, during 1944–45 famine when wheat were scarce, children symptomatically improved.3 Subsequent studies characterized many features disease, and, while pathogenesis pathophysiology remain incompletely understood, thought arise from interplay genetic, environmental immunological factors (Figure 1). Importantly, understanding pathophysiology, which trigger (wheat, barley) known, will undoubtedly reveal basic mechanisms underlie other autoimmune diseases (e.g., type I diabetes) share common pathogenic perturbations. In this review, we describe seminal findings each three domains pathogenesis: genetics, triggers immune dysregulation with focus on newer areas investigation such non-HLA genetic variants, microbiome role innate system. Open separate window Figure 1 Factors involved pathophysiology Celiac factors. This review highlights these domains.