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60 INFANT FEEDING PRACTICES AND COELIAC DISEASE Dis Child 1972; 47: 292-8. 68. Lindberg T. Coeliac disease and infant feeding practices [letter]. Lancet 1981; i: 449 69. Stenhammar L, Ansved P, Jansson G, Jansson U. The incidence of childhood celiac disease in Sweden. J Pediatr Gastroenterol Nutr 1987; 6: 707-9. 70. Kagnoff MF, Paterson YJ, Kumar PJ, Kasarda DD, Carbone FR, Unsworth DJ, et al. Evidence for the role of a human intestinal adenovirus in the pathogenesis of coeliac disease. Gut 1987; 28: 995-1001. 71. Lähdeaho ML, Parkkonen P, Reunala T, Mäki M, Lehtinen M. Antibodies to E1b proteinderived peptides of enteric adenovirus type 40 are associated with celiac disease and dermatitis herpetiformis. Clin Immunol Immunopathol 1993; 69: 300-5. 72. Howdle PD, Blair Zajdel ME, Smart CJ, Trejdosiewicz LK, Blair GE, Losowky MS. Lack of a serologic response to an E1B protein of adenovirus 12 in coeliac disease. Scand J Gastroenterol 1989; 24: 282-6. 73. Vesy CJ, Greenson JK, Papp AC, Snyder PJ, Qualman SJ, Prior TW. Evaluation of celiac disease biopsies for adenovirus 12 DNA using a multiplex polymerase chain reaction. Mod Pathol 1993; 6: 61-4. 74. Holm S, Andersson Y, Gothefors L, Lindberg T. Increased protein absorption after acute gastroenteritis in children. Acta Paediatr 1992; 81: 585-8. 75. Ivarsson A, Hernell O, Nyström L, Persson LÅ. Children born in the summer have increased risk for coeliac disease. J Epidemiol Community Health [in press]. 76. Ivarsson A. On the multifactorial etiology of celiac disease: An epidemiological approach to the Swedish epidemic. Department of Clinical Sciences, Pedatrics, Umeå University, Sweden. [Dissertation] 2001. 77. Rothman KJ, Greenland S. Causation and causal inference. In: Rothman KJ, Greenland S, eds. Modern epidemiology: 2nd ed. Lippincott - Raven, Philadelphia: 1998; 7-28. 78. ESPGAN committee on nutrition. Guidelines on infant nutrition III. Recommendations for infant feeding. Acta Paediatr Scand Suppl 1982; 302: 16-20. 79. Hallert C, Gotthard R, Jansson G, Norrby K, Walan A. Similar prevalence of coeliac disease in children and middle-aged adults in a district of Sweden. Gut 1983; 24: 389-91.
Catassi C, Fasano A, Corazza GR (eds): Primary prevention of coeliac disease. The utopia of the new millennium? Perspectives on Coeliac Disease, vol. 1, AIC Press, pp 61-73 Mechanisms of oral tolerance - lessons for coeliac disease? Conleth Feighery Department of Immunology, Trinity College Dublin and St. James's Hospital, Dublin, Ireland Introduction Coeliac disease (CD) is an inflammatory disease of the upper small intestine and 1 results from gluten ingestion in genetically susceptible individuals . Gluten is the essential environmental factor in the development of CD: this is demonstrated by the clinical and mucosal recovery which follows the institution of a gluten-free diet. Genetic factors also play a critical role in the development of CD and a strong association with certain Major Histocompatibility Complex (MHC) class II genes 2 (HLA-DQ2 and HLA-DQ8) is well established . However, CD is a polygenic disorder and many additional genes, yet to be identified, also contribute to the pathogenesis of CD. There is no evidence to suggest that these genes are in any sense “abnormal” and similar genetic polymorphisms are well represented in the normal population. Since gluten is part of the normal stable diet, and the genes which permit the development of CD are present in the normal population, the question can be reasonably posed - what makes a particular individual susceptible to gluten induced damage? It is speculated that additional factors, for example infectious agents and sex hormones, may be involved. Other environmental factors may also contribute but currently there are few clues as to what these are. This leads to the broader issue how does the gut immune system “view” foods? Foods of their essence are foreign proteins and as such might be targeted for elimination, as is the case with any other foreign antigen. CD is a common disorder. According to current evidence, it may affect 0.5 to 1% of 3-4 the population . This suggests that gluten has unique, but ill-understood, properties which frequently results in a T cell, delayed-type hypersensitivity response to this food antigen. There is little evidence that other food proteins cause a similar reaction. In contrast, many foods stimulate food allergy, a type I hypersensitivity reaction with 5 specific IgE production to the offending antigen . In food allergy, a systemic reaction to 61
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Perspectives on Coeliac Disease Vol
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The AIC Meeting was held in the Aul
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Italian Coeliac Society, Via Picott
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Preface Coeliac disease (CD) is a u
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Contents Current understanding of t
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2 THE BASIS OF COELIAC DISEASE hapl
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4 THE BASIS OF COELIAC DISEASE 1 pr
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6 THE BASIS OF COELIAC DISEASE spre
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8 THE BASIS OF COELIAC DISEASE Ackn
Page 24 and 25: 10 THE BASIS OF COELIAC DISEASE glu
Page 27 and 28: Catassi C, Fasano A, Corazza GR (ed
Page 29: T CELL RESPONSES TO GLUTEN PEPTIDES
Page 32 and 33: 18 A DOMINANT EPITOPE IN GLUTEN PEP
Page 42 and 43: 28 ROLE OF A-GLIADIN 31-49 PEPTIDE
Page 47 and 48: COELIAC DISEASE IN THE SAHARAWI 33
Page 55: COELIAC DISEASE IN THE SAHARAWI 41
Page 58 and 59: 44 INFANT FEEDING PRACTICES AND COE
Page 66 and 67: Age (years) 52 INFANT FEEDING PRACT
Page 76 and 77: 62 MECHANISMS OF ORAL TOLERANCE the
Page 78 and 79: 64 MECHANISMS OF ORAL TOLERANCE pot
Page 80 and 81: 66 MECHANISMS OF ORAL TOLERANCE Epi
Page 82 and 83: 68 MECHANISMS OF ORAL TOLERANCE typ
Page 84 and 85: 70 MECHANISMS OF ORAL TOLERANCE 51
Page 86 and 87: 72 MECHANISMS OF ORAL TOLERANCE 23.
Page 91 and 92: GENETICALLY DETOXIFIED GRAINS 77 to
Page 93 and 94: • • GENETICALLY DETOXIFIED GRAI
Page 95 and 96: GENETICALLY DETOXIFIED GRAINS 81 3.
Page 99 and 100: IMMUNOTHERAPY OF COELIAC DISEASE 85
Page 101 and 102: IMMUNOTHERAPY OF COELIAC DISEASE 87
Page 105 and 106: RECENT ADVANCES ON GLUTEN TOXICITY
Page 107 and 108: Index A Antiendomysium antibodies (
Page 109: INDEX 95 W Wheat, 7, 23, 27, 31, 53
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