Celiac disease: pathogenesis of a model immunogenetic disease

被引:242
作者
Kagnoff, Martin F.
机构
[1] Univ Calif San Diego, Wm K Warren Med Res Ctr Celiac Dis, La Jolla, CA 92093 USA
[2] Univ Calif San Diego, Lab Mucosal Immunol, Dept Med, La Jolla, CA 92093 USA
[3] Univ Calif San Diego, Lab Mucosal Immunol, Dept Pediat, La Jolla, CA 92093 USA
关键词
D O I
10.1172/JCI30253
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Celiac disease is characterized by small-intestinal mucosal injury and nutrient malabsorption in genetically susceptible individuals in response to the dietary ingestion of wheat gluten and similar proteins in barley and rye. Disease pathogenesis involves interactions among environmental, genetic, and immunological factors. Although celiac disease is predicted by screening studies to affect approximately 1% of the population of the United States and is seen both in children and in adults, 10%/15% or fewer of these individuals have been diagnosed and treated. This article focuses on the role of adaptive and innate immune mechanisms in the pathogenesis of celiac disease and how current concepts of immunopathogenesis might provide alternative approaches for treating celiac disease.
引用
收藏
页码:41 / 49
页数:9
相关论文
共 97 条
[61]   Genome-wide linkage analysis for celiac disease in North American families [J].
Neuhausen, SL ;
Feolo, M ;
Camp, NJ ;
Farnham, J ;
Book, L ;
Zone, JJ .
AMERICAN JOURNAL OF MEDICAL GENETICS, 2002, 111 (01) :1-9
[62]   Gluten induces an intestinal cytokine response strongly dominated by interferon gamma in patients with celiac disease [J].
Nilsen, EM ;
Jahnsen, FL ;
Lundin, KEA ;
Johansen, FE ;
Fausa, O ;
Sollid, LM ;
Jahnsen, J ;
Scott, H ;
Brandtzaeg, P .
GASTROENTEROLOGY, 1998, 115 (03) :551-563
[63]  
Pender SLF, 1997, J IMMUNOL, V158, P1582
[64]   Saturation of the 5q3l-q33 candidate region for coeliac disease [J].
Percopo, S ;
Babron, MC ;
Whalen, M ;
De Virgiliis, S ;
Coto, I ;
Clerget-Darpoux, F ;
Landolfo, F ;
Greco, L .
ANNALS OF HUMAN GENETICS, 2003, 67 :265-268
[65]   Effect of prolyl endopeptidase on digestive-resistant gliadin peptides in vivo [J].
Piper, JL ;
Gray, GM ;
Khosla, C .
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2004, 311 (01) :213-219
[66]   ON THE HLA-DQ(ALPHA-1-ASTERISK-0501, BETA-1-ASTERISK-0201)-ASSOCIATED SUSCEPTIBILITY IN CELIAC-DISEASE - A POSSIBLE GENE DOSAGE EFFECT OF DQB1-ASTERISK-0201 [J].
PLOSKI, R ;
EK, J ;
THORSBY, E ;
SOLLID, LM .
TISSUE ANTIGENS, 1993, 41 (04) :173-177
[67]   Genome screening of coeliac disease [J].
Popat, S ;
Bevan, S ;
Braegger, CP ;
Busch, A ;
O'Donoghue, D ;
Falth-Magnusson, K ;
Godkin, A ;
Hogberg, L ;
Holmes, G ;
Hosie, KB ;
Howdle, PD ;
Jenkins, H ;
Jewell, D ;
Johnston, S ;
Kennedy, NP ;
Kumar, P ;
Logan, RFA ;
Love, AHG ;
Marsh, MN ;
Mulder, CJ ;
Sjoberg, K ;
Stenhammar, L ;
Walker-Smith, J ;
Houlston, RS .
JOURNAL OF MEDICAL GENETICS, 2002, 39 (05) :328-331
[68]   HISTOLOGICAL-CHANGES IN SMALL-BOWEL MUCOSA INDUCED BY GLIADIN SENSITIVE T-LYMPHOCYTES CAN BE BLOCKED BY ANTIINTERFERON-GAMMA ANTIBODY [J].
PRZEMIOSLO, RT ;
LUNDIN, KEA ;
SOLLID, LM ;
NELUFER, J ;
CICLITIRA, PJ .
GUT, 1995, 36 (06) :874-879
[69]   Refining the rules of gliadin T cell epitope binding to the disease-associated DQ2 molecule in celiac disease: Importance of proline spacing and glutamine deamidation [J].
Qiao, SW ;
Bergseng, E ;
Molberg, O ;
Jung, G ;
Fleckenstein, B ;
Sollid, LM .
JOURNAL OF IMMUNOLOGY, 2005, 175 (01) :254-261
[70]   Antigen presentation to celiac lesion-derived T cells of a 33-mer gliadin peptide naturally formed by gastrointestinal digestion [J].
Qiao, SW ;
Bergseng, E ;
Molberg, O ;
Xia, J ;
Fleckenstein, B ;
Khosla, C ;
Sollid, LM .
JOURNAL OF IMMUNOLOGY, 2004, 173 (03) :1757-1762