New aspects in celiac disease

被引：31
作者：
Torres, M. I.
Lopez Casado, M. A.
Rios, A.
机构：
[1] Univ Jaen, Dept Expt Biol, Jaen 23071, Spain
[2] Hosp Virgen de las Nieves, Dept Pediat Gastroenterol, Granada, Spain
[3] Univ Granada, Dept Cell Biol, Granada, Spain
来源：
WORLD JOURNAL OF GASTROENTEROLOGY | 2007年 / 13卷 / 08期
关键词：
celiac disease; oral tolerance; IL-10; TGF-beta; gluten intolerance;
D O I：
10.3748/wjg.v13.i8.1156
中图分类号：
R57 [消化系及腹部疾病];
学科分类号：
摘要：
Celiac disease (CD) is a common autoimmune disorder characterized by an immune response to ingested gluten and has a strong HLA association with HLA-DQ2 and HLA-DQ8 molecules, but human HLA-DQ risk factors do not explain the entire genetic susceptibility to gluten intolerance. CD is caused by the lack of immune tolerance (oral tolerance) to wheat gluten. In this sense, the expression of soluble HLA-G in CD is of special interest because the molecule plays an important role in the induction of immune tolerance. The enhanced expression of soluble HLA-G found in CD may be part of a mechanism to restore the gluten intolerance. In this editorial, we review recent progress in understanding CD in relation to its prevalence, diagnosis and possible mechanisms of pathogenesis., (C) 2007 The WJG Press. All rights reserved.
引用
收藏
页码：1156 / 1161
页数：6
相关论文
共 45 条
[21]   Structural basis for HLA-DQ2-mediated presentation of gluten epitopes in celiac disease [J].
Kim, CY ;
Quarsten, H ;
Bergseng, E ;
Khosla, C ;
Sollid, LM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (12) :4175-4179
[22]   Indoleamine 2,3 dioxygenase and human leucocyte antigen-G inhibit the T-cell alloproliferative response through two independent pathways [J].
Le Rond, S ;
Gonzalez, A ;
Gonzalez, ASL ;
Carosella, ED ;
Rouas-Freiss, N .
IMMUNOLOGY, 2005, 116 (03) :297-307
[23]  
LI L, 1994, J IMMUNOL, V153, P3967
[24]   A gene telomeric of the HLA class I region is involved in predisposition to both type 1 diabetes and coeliac disease [J].
Lie, BA ;
Sollid, LM ;
Ascher, H ;
Ek, J ;
Akselsen, HE ;
Ronningen, KS ;
Thorsby, E ;
Undlien, DE .
TISSUE ANTIGENS, 1999, 54 (02) :162-168
[25]   Soluble HLA-G protein secreted by allo-specific CD4+ T cells suppresses the allo-proliferative response:: A CD4+ T cell regulatory mechanism [J].
Lila, N ;
Rouas-Freiss, N ;
Dausset, J ;
Carpentier, A ;
Carosella, ED .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (21) :12150-12155
[26]   TNFα, IFNγ and IL-10 gene polymorphisms in a sample of Sicilian patients with coeliac disease [J].
Lio, D ;
Scola, L ;
Forte, GI ;
Accomando, S ;
Giacalone, A ;
Crivello, A ;
Cataldo, F .
DIGESTIVE AND LIVER DISEASE, 2005, 37 (10) :756-760
[27]   HLA in coeliac disease: Unravelling the complex genetics of a complex disorder [J].
Louka, AS ;
Sollid, LM .
TISSUE ANTIGENS, 2003, 61 (02) :105-117
[28]   T-CELLS FROM THE SMALL-INTESTINAL MUCOSA OF A DR4,DQ7 DR4,DQ8 CELIAC-DISEASE PATIENT PREFERENTIALLY RECOGNIZE GLIADIN WHEN PRESENTED BY DQ8 [J].
LUNDIN, KEA ;
SCOTT, H ;
FAUSA, O ;
THORSBY, E ;
SOLLID, LM .
HUMAN IMMUNOLOGY, 1994, 41 (04) :285-291
[29]   Interleukin 15 mediates epithelial changes in celiac disease [J].
Maiuri, L ;
Ciacci, C ;
Auricchio, S ;
Brown, V ;
Quaratino, S ;
Londei, M .
GASTROENTEROLOGY, 2000, 119 (04) :996-1006
[30]  
MCMASTER MT, 1995, J IMMUNOL, V154, P3771
12345