Mechanisms of Disease: immunopathogenesis of celiac disease

被引:133
作者
Jabri, Bana [1 ]
Sollid, Ludvig M.
机构
[1] Univ Chicago, Dept Pathol Med & Pediat, Chicago, IL 60637 USA
[2] Univ Oslo, N-0316 Oslo, Norway
[3] Rikshop Univ Hosp, Rikshosp, Radiumhosp Med Ctr, Oslo, Norway
来源
NATURE CLINICAL PRACTICE GASTROENTEROLOGY & HEPATOLOGY | 2006年 / 3卷 / 09期
关键词
celiac disease; gluten; major histocompatibility complex; natural killer receptors; transglutaminase;
D O I
10.1038/ncpgasthep0582
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Celiac disease is a genetic inflammatory disorder with autoimmune components that is induced by the ingestion of dietary gluten. Refractory sprue and enteropathy-associated T-cell lymphoma are rare but distinctive complications of the disease. Although the importance of the adaptive immune response to gluten has been well established, observations now also point towards a central role for the gluten-induced innate stress response in the pathogenesis of celiac disease and its malignant complications.
引用
收藏
页码:516 / 525
页数:10
相关论文
共 79 条
[1]   Cell surface tissue transglutaminase is involved in adhesion and migration of monocytic cells on fibronectin [J].
Akimov, SS ;
Belkin, AM .
BLOOD, 2001, 98 (05) :1567-1576
[2]   Association analysis of MYO9B gene polymorphisms with celiac disease in a Swedish/Norwegian cohort [J].
Amundsen, SS ;
Monsuur, AJ ;
Wapenaar, MC ;
Lie, BA ;
Ek, J ;
Gudjónsdóttir, AH ;
Ascher, H ;
Wijmenga, C ;
Sollid, LM .
HUMAN IMMUNOLOGY, 2006, 67 (4-5) :341-345
[3]   The molecular basis for oat intolerance in patients with Celiac disease [J].
Arentz-Hansen, H ;
Fleckenstein, B ;
Molberg, O ;
Scott, H ;
Koning, F ;
Jung, G ;
Roepstorff, P ;
Lundin, KEA ;
Sollid, LM .
PLOS MEDICINE, 2004, 1 (01) :84-92
[4]   Meta and pooled analysis of European coeliac disease data [J].
Babron, MC ;
Nilsson, S ;
Adamovic, S ;
Naluai, ÅT ;
Wahlström, J ;
Ascher, H ;
Ciclitira, PJ ;
Sollid, LM ;
Partanen, J ;
Greco, L ;
Clerget-Darpoux, F .
EUROPEAN JOURNAL OF HUMAN GENETICS, 2003, 11 (11) :828-834
[5]   Activation of NK Cells and T Cells by NKG2D, a Receptor for Stress-Inducible MICA [J].
Bauer, Stefan ;
Groh, Veronika ;
Wu, Jun ;
Steinle, Alexander ;
Phillips, Joseph H. ;
Lanier, Lewis L. ;
Spies, Thomas .
JOURNAL OF IMMUNOLOGY, 2018, 200 (07) :2231-2233
[6]   HLA-E binds to natural killer cell receptors CD94/NKG2A, B and C [J].
Braud, VM ;
Allan, DSJ ;
O'Callaghan, CA ;
Söderström, K ;
D'Andrea, A ;
Ogg, GS ;
Lazetic, S ;
Young, NT ;
Bell, JI ;
Phillips, JH ;
Lanier, LL ;
McMichael, AJ .
NATURE, 1998, 391 (6669) :795-799
[7]   TACI is mutant in common variable immunodeficiency and IgA deficiency [J].
Castigli, E ;
Wilson, SA ;
Garibyan, L ;
Rachid, R ;
Bonilla, F ;
Schneider, L ;
Geha, RS .
NATURE GENETICS, 2005, 37 (08) :829-834
[8]   Prevalence and clinical features of selective immunoglobulin A deficiency in coeliac disease: an Italian multicentre study [J].
Cataldo, F ;
Marino, V ;
Ventura, A ;
Bottaro, G ;
Corazza, GR .
GUT, 1998, 42 (03) :362-365
[9]   The coeliac iceberg in Italy. A multicentre antigliadin antibodies screening for coeliac disease in school-age subjects [J].
Catassi, C ;
Fabiani, E ;
Ratsch, IM ;
Coppa, GV ;
Giorgi, PL ;
Pierdomenico, R ;
Alessandrini, S ;
Iwanejko, G ;
Domenici, R ;
Mei, E ;
Miano, A ;
Marani, M ;
Bottaro, G ;
Spina, M ;
Dotti, M ;
Montanelli, A ;
Barbato, M ;
Viola, F ;
Lazzari, R ;
Vallini, M ;
Guariso, G ;
Plebani, M ;
Cataldo, F ;
Traverso, G ;
Ughi, C ;
Chiaravalloti, G ;
Baldassarre, M ;
Scarcella, P ;
Bascietto, F ;
Ceglie, L ;
Valenti, A ;
Paolucci, P ;
Caradonna, M ;
Bravi, E ;
Ventura, A .
ACTA PAEDIATRICA, 1996, 85 :29-35
[10]   Refractory sprue, coeliac disease, and enteropathy-associated T-cell lymphoma [J].
Cellier, C ;
Delabesse, E ;
Helmer, C ;
Patey, N ;
Matuchansky, C ;
Jabri, B ;
Macintyre, E ;
Cerf-Bensussan, N ;
Brousse, N .
LANCET, 2000, 356 (9225) :203-208