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70 MECHANISMS OF ORAL TOLERANCE 51 intolerance is a central feature of the disorder . However, in the past, cases of possible 52 transient gluten sensitivity were described . Is it possible that this phenomenon of 53-54 transiency is more common than currently appreciated? . The events that happen to pediatric cases of CD, when they reach adolescence, may be informative concerning the permanency of gluten intolerance. Detailed information about these events is absent. Nonetheless, it is recognized that many children adhere less well to a strict gluten free diet when they reach adolescence. This may represent the general “rebellion” of teenagers! Despite eating gluten containing foods, few symptoms may develop. This in turn may lead to increasing carelessness about their diets. Some of these patients eventually have intestinal biopsies performed and the mucosa can appear surprisingly normal or even completely normal. Doubts about the accuracy of the initial diagnosis of CD may then be raised. Some of these patients are then given a gluten challenge and it is reported that it can take many months or even 55-56 years for histological evidence of CD to return . This contrasts with gluten challenge in patients with an adult diagnosis of CD when symptomatic and histological evidence 56 of disease relapse often only requires one or two months of gluten intake . Although categorical data about adolescent remission of CD is lacking, the information available strongly suggests that this really does occur. If this is the case, it may indicate that restoration of tolerance to gluten is possible. The majority, if not all of these patients, eventually develop symptomatic gluten intolerance in adulthood, demonstrating the essential permanency of CD. However, it is possible that investigation of adolescent CD patients, during their period of remission, may give insight to T cell tolerance mechanisms towards gluten. Conclusions The gut mucosal immune response to the majority of food and other antigens is typically of low intensity and remains confined to the local environment. The term ²oral tolerance²may be applied to this controlled immune response. However, in the case of a single food type, gluten, an enhanced T cell immune response develops in a substantial number of individuals and features of coeliac disease develop. In this disorder, immune tolerance of gluten is apparently lost. With an improved understanding of the mechanisms of oral tolerance, it is possible that manipulation of the immune response to gluten in coeliac patients could restore the normal physiological state of low reactivity to this food antigen. This would remove the requirement of gluten-free diet treatment of coeliac disease. References 1. Feighery C. Coeliac disease Fortnightly review. BMJ 1999; 319: 236-9. 2. Kagnoff MF. Genetic basis of Coeliac Disease: role of HLA genes. In: MN Marsh (Ed) Coeliac Disease, Oxford, Blackwell Scientific Publications, 1992; pp215-38. 3. Catassi C, Fabiani E, Rätsch IM, Coppa GV, Giorgi PL, Pierdomenico R, et al. The coeliac iceberg in Italy. A multicentre antigliadin antibodies screening for coeliac disease in school-age subjects. Acta Paediatr Suppl 1996; 412: 29-35. 4. McMillan SA, Watson RPG, McCrum EE, Evans AE. Factors associated with serum
MECHANISMS OF ORAL TOLERANCE 71 antibodies to reticulin, endomysium, and gliadin in an adult population. Gut 1996; 39: 43-7. 5. Furukawa CT. Adverse Reactions to Food. In: Allergy in Primary Care. Eds. LC. Altman, JW. Becker, PV Williams. Publishers. W.B. Saunders Company 2000; 18: 259-64. 6. Sampson HA. What should we be doing for children with peanut allergy? J Pediatr 2000; 137: 741-3. 7. Kamradt T, Mitchison NA. Tolerance and Autoimmunity. N Engl J Med 2001; 344: 655-64. 8. Bibel DJ. Milestones in Immunology: a historical exploration. Science Tech Publishers, Wisconsin, USA. 1988. 9. Janeway CA, Travers P, Walport M, Capra JD. Immunobiology: the immune system in health and disease. Churchill Livingstone, 1999. 10. Davidson A, Diamond B. Advances in Immunology: Autoimmune Diseases. N Engl J Med 2001; 345: 340-50. 11. Shevach EM. Certified Professionals: CD4+ CD25+ Suppressor T Cells. J Exp Med 2001; 193: F41-5. 12. Feighery C. Intestinal Immune System - A Hidden Symphony. In: Gastrointestinal Immunology and Gluten-Sensitive Disease. Proceedings of the Sixth International Symposium on Coeliac Disease held at Trinity College, Dublin in July 1992. Eds. C. Feighery, C. O'Farrelly, Publishers Oak Tree Press, Dublin. 13. Brandtzaeg P, Baekkevold ES, Farstad IN, Jahnsen FL, Johansen FE, Nilsen EM, et al. Regional specialization in the mucosal immune system: what happens in the microcompartments? Immunol Today 1999; 3: 141-51. 14. Garside P, Mowat AM, Khoruts A. Oral tolerance in disease. Gut 1999; 44: 137-42. 15. Weiner HL. Induction and mechanism of action of transforming growth factor-betasecreting Th3 regulatory cells. Immunol Rev 2001; 182: 207-14. 16. Mowat McI A. The regulation of immune responses to dietary protein antigens. Immunology Today 1987; 8: 93-8. 17. Dicke WK. Coeliakie. PhD thesis. University of Utreacht, Utreacht, The Netherlands, 1950. 18. Lamont AG, Mowat AM, Parrott DM. Priming of systemic and local delayed-type hypersensitivity responses by feeding low doses of ovalbumin to mice. Immunology 1989; 66: 595-9. 19. Fry L. Dermatitis herpetiformis: from gut to skin, contributions to the nature of coeliac disease. In: Coeliac Disease, Mäki M, Collin P, Visakorpi JK (eds). Proceedings of the Seventh International Symposium on Coeliac Disease, Finland. Publishers. Coeliac Disease Study Group, Tampere, Finland,1996; pp67-74. 20. Cronin CC, Jackson LM, Feighery C, Shanahan F, Abuzakouk M, Ryder DQ, et al. Coeliac disease and epilepsy. Q J Med 1998; 91: 303-8. 21. Hadjivassiliou M, Grunewald RA, Chattopadhyay AK, Davies-Jones GA, Gibson A, Jarratt JA et al. Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia. Lancet 1998; 352: 1582-5. 22. Ensari A, Marsh MN, Loft DE, Morgan S, Moriarty K. Morphometric analysis of intestinal mucosa. V. Quantitative histological and immunocytochemical studies of rectal mucosae in gluten sensitivity. Gut 1993; 34: 1225-9.
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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
Page 34 and 35: 20 A DOMINANT EPITOPE IN GLUTEN PEP
Page 42 and 43: 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
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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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