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乳糜泻的分子基础。

The molecular basis of celiac disease.

作者信息

Koning Frits

机构信息

Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands.

出版信息

J Mol Recognit. 2003 Sep-Oct;16(5):333-6. doi: 10.1002/jmr.641.

DOI:10.1002/jmr.641
PMID:14523946
Abstract

Celiac disease is caused by inflammatory, gluten specific T cell responses in the small intestine. Invariably such responses are HLA-DQ2 or HLA-DQ8 restricted, providing an explanation for the strong association between celiac disease and these HLA-class II alleles. It is now clear that some native gluten sequences can bind to HLA-DQ2/8 and induce T cell responses. In addition, modification of gluten peptides by the enzyme tissue transglutaminase results in high affinity HLA-DQ2/8 binding peptides that can induce T cell responses. Thus, gluten molecules contain a large number of immunogenic peptides and this is likely to play an important role in the breaking of oral tolerance to gluten.

摘要

乳糜泻由小肠中针对麸质的炎症性T细胞反应引起。这些反应无一例外受HLA - DQ2或HLA - DQ8限制,这就解释了乳糜泻与这些HLA - II类等位基因之间的强关联。现在已经明确,一些天然麸质序列可与HLA - DQ2/8结合并诱导T细胞反应。此外,组织转谷氨酰胺酶对麸质肽的修饰会产生能诱导T细胞反应的高亲和力HLA - DQ2/8结合肽。因此,麸质分子包含大量免疫原性肽,这可能在打破对麸质的口服耐受性中起重要作用。

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