Pathophysiology and immunogenetics of celiac disease

被引：20

作者：

Aboulaghras, Sara ^{[1
,3
]}

Piancatelli, Daniela ^{[2
]}

Oumhani, Khadija ^{[3
]}

Balahbib, Abdelaali ^{[4
]}

Bouyahya, Abdelhakim ^{[5
]}

Taghzouti, Khalid ^{[1
]}

机构：

[1] Mohammed V Univ Rabat, Fac Sci Genom Human Pathol Res, Genom Human Pathol Res, Physiol & Physiopathol Team, Rabat, Morocco

[2] Natl Res Council CNR, Inst Translat Pharmacol IFT, Laquila, Italy

[3] Inst Natl Hyg, Lab Immunol, Rabat, Morocco

[4] Mohammed V Univ Rabat, Fac Sci, Lab Zool & Gen Biol, Rabat, Morocco

[5] Mohammed V Univ Rabat, Fac Sci, Genom Ctr Human Pathol Res, Dept Biol,Lab Human Pathol Biol, Rabat, Morocco

来源：

CLINICA CHIMICA ACTA | 2022年 / 528卷

关键词：

Celiac disease; HLA; Physiopathology; Transglutaminase; 2; Microbiota; RESTRICTED T-CELLS; GLUTEN-FREE DIET; TISSUE TRANSGLUTAMINASE; HLA-DQ; INTERFERON-GAMMA; GUT MICROBIOTA; INTESTINAL PERMEABILITY; STORAGE PROTEINS; GLIADIN; PREVALENCE;

D O I：

10.1016/j.cca.2022.01.022

中图分类号：

R446 [实验室诊断]; R-33 [实验医学、医学实验];

学科分类号：

1001 ;

摘要：

Celiac disease (CD) is a chronic inflammatory enteropathy caused by gluten (protein from wheat, rye and, barley) in genetically predisposed individuals carrying the HLA-DQ2/HLA-DQ8 genotype. This pathology has a multi factorial etiology in which HLA genes, the microbiome, gluten and, other environmental factors are involved in the development of the disease. Its pathogenesis involves both innate and adaptive immunity as well as upregulation of IL-15. The objective of this review is to examine the results of current studies on genetic and environmental variables to better understand the pathogenesis of this enteropathy. The complex etiology of celiac disease makes our understanding of the pathogenesis of the disease incomplete, and a better knowledge of the many genetic and environmental components would help us better understand the pathophysiology of celiac disease.

引用

页码：74 / 83

页数：10

共 148 条

[71] Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3 [J].