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82 GENETICALLY DETOXIFIED GRAINS strategy used by diverse DNA and RNA viruses of plants. Proc Natl Acad Sci 1999;96:14147-52. 21. Blechl AE, Anderson OD. Expression of a novel high-molecular-weight glutenin subunit gene in transgenic wheat. Nat Biotechnol 1996;14:875-9. 22. Barro F, Rooke L, Békés F, Gras P, Tatham AS, Fido R, et al. Transformation of wheat with high molecular weight subunit genes results in improved functional properties. Nat Biotechnol 1997;15:1295-9. 23. Altpeter F, Vasil V, Srivastava V, Vasil IK. Integration and expression of the highmolecular-weight glutenin subunit 1Ax1 gene into wheat. Nat Biotechnol 1996;14:1155-9. 24. Srivastava V, Anderson OD, Ow DW. Single-copy transgenic wheat generated through the resolution of complex integration patterns. Proc Natl Acad Sci. USA. 1999;96:11117-21.
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 83-88 Immunotherapy of coeliac disease: where do we stand? 1 1 1 1 Carmen Gianfrani , Mauro Rossi , Giuseppe Mazzarella , Francesco Maurano , 2 2 2 2 Virginia Salvati , Delia Zanzi , Salvatore Auricchio and Riccardo Troncone 1 2 Institute of Food Sciences and Technology, CNR, Avellino, Italy; Department of Pediatrics and European Laboratory for Food-Induced Disease, University Federico II, Naples, Italy Introduction Coeliac Disease (CD) is with little doubt an immune-mediated disease, triggered by the ingestion of wheat gliadin and related prolamines from other toxic cereal such as barley and rye. The hallmark of CD is the enteropathy characterized by an altered morphology of villous architecture and severe malabsorption, but it is now very clear 1 that the disease affects not only the small intestine . An important feature of CD is its strong genetic association with HLA class II genes: more than 90% of patients carry the HLA-DQA*0501/DQB*0201 (DQ2) alleles, whereas the majority of DQ2-negative patients are DQ8-positive 2 (DQA*0301/DQB*0302) . Among the non HLA genes that have been suggested to contribute to the CD susceptibility so far, only the CTLA4 gene has been found associated to coeliac disease in several populations examined. The strong genetic association with HLA molecules is strengthened by the finding that gliadin-derived peptides are recognized by coeliac intestinal lymphocytes when presented by the disease predisposing DQ2 or DQ8 molecules. In fact, from the immunological point of view, it is now generally accepted that a recognition of gliadin peptides in association with HLA Class II molecules by Th1 T cells secreting proinflammatory cytokine leads 3 to the overt CD lesions at the intestinal level . CD, in the great majority of cases, is efficiently cured by the gluten-free diet; nevertheless, for some patients the diet is unpalatable and for others the compliance is quite poor. For these reasons a more acceptable form of therapy would be desirable: many efforts from our laboratory are focused on the development of conceptually amenable therapeutic strategies. In particular, considering that CD is an immune mediated pathology, any immunomodulatory strategy that could specifically block the adverse immune reactions triggered by gliadin, represents a valid alternative to the exclusion diet. Moreover, because the dietetic approach has a proven efficacy and safety, the immunomodulatory therapy must be strictly antigen-specific, not affecting the immune response to other antigens, and devoid of risks. 83
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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
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10 THE BASIS OF COELIAC DISEASE glu
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Catassi C, Fasano A, Corazza GR (ed
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T CELL RESPONSES TO GLUTEN PEPTIDES
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18 A DOMINANT EPITOPE IN GLUTEN PEP
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28 ROLE OF A-GLIADIN 31-49 PEPTIDE
Page 45 and 46: Catassi C, Fasano A, Corazza GR (ed
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: 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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