观察HLA-DQ2、饮食暴露和乳糜泻对儿童谷蛋白抗体形成中的诱导作用

作     者：Ludvigsson J. Eylert M. Ilonen J. O.Vaarala 沙焕臣 

作者机构：Department of Molecular and Clinical MedicineFaculty of Health SciencesLinkping UniversitySweden 

出 版 物：《世界核心医学期刊文摘（胃肠病学分册）》 (Core Journals in Gastroenterology)

年 卷 期：2006年第2卷第12期

页      面：54-55页

学科分类：1002[医学-临床医学] 100202[医学-儿科学] 10[医学] 

主　　题：HLA-DQ2 抗体形成 乳糜泻 谷蛋白 体液免疫应答 β-乳球蛋白 蛋白抗体 组织学检查 抗体反应 

摘      要：*** study the effect of HLA DQ2,dietary history and development of coeliac disease(CD) on the induction of antibody response to wheat gliadin and cow’s milk,beta-lactoglobulin between 1 and 2.5 years of age in children who developed CD and in healthy *** and *** participating in a birth cohort study(the ABIS study) in Sweden were ***-nine children developed CD(cases) ,confirmed through biopsy,during follow-up until 2.5-5 years of age.A total of 181 healthy control children were matched for duration of exclusive breast-feeding,birth-weight,gender,maternal smoking and season of *** and IgA antigliadin and anti-beta-lactoglobulin antibodies were measured using enzyme immunoassay(EIA) .The effects of HLA-risk genotypes,DQ2 and DQ8,on CD were also *** who developed CD had higher IgG and IgA antigliadin and anti-beta-lactoglobulin antibody levels at 1 year of age than controls(all comparisons:p 0.001) .Similar differences were seen between cases with as yet undiagnosed CD by 1 year of age and controls,and also when cases were compared with HLA-matched *** levels of IgG and IgA antibodies to beta-lactoglobu-lin(p = 0.003;p = 0.001) ,but not to gliadin,were found in treated cases versus controls at 2.5 years of ***-DQ2-positive healthy children had lower levels of IgG and IgA antigliadin antibodies than HLADQ2 negative controls at 1 year of age(p = 0.004;p = 0.012) .*** humoral response emerging not only to gliadin,but also to other food antigens seems to be primarily associated with *** induction of antibody response to wheat gliadin in healthy children with the HLA-DQ2 risk molecule could at least partly explain the genetic predisposition to gluten intolerance and CD.