Arranz Eduardo, Garrote José A
Laboratorio de Inmunología de las Mucosas, Instituto de Biología y Genética Molecular (IBGM), Universidad de Valladolid-CSIC, Valladolid, España.
Gastroenterol Hepatol. 2010 Nov;33(9):643-51. doi: 10.1016/j.gastrohep.2009.11.003. Epub 2010 Feb 2.
Celiac disease is an inflammatory disorder of the small intestine induced by intake of wheat gluten and other prolamines in genetically susceptible individuals. This disease is manifested by an increased number of intraepithelial and lamina propria lymphocytes, villous atrophy, tissue remodeling and the presence of anti-transglutaminase antibodies. The most widely accepted pathogenic model is based on adaptive immunity after T CD4(+)lymphocyte stimulation by tissue transglutamine-modified gluten peptides and HLA-DQ2/DQ8 restriction, which produce proinflammatory cytokines. Gluten also activates innate immunity and epithelial cytotoxicity mediated by intraepithelial lymphocytes. Although the effect of specific antibodies remains unclear, the availability of serological and immunogenetic markers as diagnostic tools has increased our knowledge of celiac disease and has led to a reevaluation of the diagnostic criteria, especially in adults with minimal or atypical disease expression.
乳糜泻是一种在遗传易感性个体中，由摄入小麦麸质和其他醇溶蛋白引发的小肠炎症性疾病。这种疾病表现为上皮内淋巴细胞和固有层淋巴细胞数量增加、绒毛萎缩、组织重塑以及抗转谷氨酰胺酶抗体的存在。目前最被广泛接受的致病模型基于组织转谷氨酰胺修饰的麸质肽刺激T CD4(+)淋巴细胞后产生的适应性免疫以及HLA - DQ2/DQ8限制，进而产生促炎细胞因子。麸质还会激活由上皮内淋巴细胞介导的固有免疫和上皮细胞毒性。尽管特异性抗体的作用仍不明确，但血清学和免疫遗传学标志物作为诊断工具的可用性增加了我们对乳糜泻的认识，并促使对诊断标准进行重新评估，尤其是在疾病表现轻微或不典型的成人患者中。
