primary prevention of coeliac disease - Associazione Italiana ...

More documents

Recommendations

Info

88 IMMUNOTHERAPY OF COELIAC DISEASE al. Antigen analog-major histocompatibily complexes act as antagonist of the T cell receptor. Cell 1992; 68: 625. 13. Arentz-Hansen H, Korner R, Molberg O, Quarsten H, Vader W, Kooy Y, et al. The intestinal T cell response to a-gliadin in adult celiac disease is focused on a single deamidated glutamine targeted by tissue transglutaminase. J Exp Med 2000; 191: 603-12. 14. van de Wal Y, Kooy Y, van Veelen PA, Pena SA, Mearin ML, Molberg O, et al. Small intestinal T cells of celiac disease patients recognize a natural pepsin fragment of gliadin. Proc Natl Acad Sci U S A 1998; 95: 10050-4. 15. Sjostrom H, Lundin K, Molberg O, Korner R, McAdam S, Anthonsen D, et al. Identification of a gliadin T-cell epitope in coeliac disease: general importance of gliadin deamidation for intestinal T-cell recognition. Scand J Immunol 1998; 48: 111-5. 16. van de Wal Y. Kooy Y. van Veelen P.A. Vader W. August SA. Drijfhout J. Pena S.A. Koning F. Glutenin is involved in the gluten-driven mucosal T cell response. Eur J Immunol 1999; 29: 3133-39. 17. Molberg O, McAdam S, Lundin KEA, Kristiansen C, Arentz-Hansen H, Kett K, et al. T cell from coeliac disease lesions recognize gliadin epitopes deamidated in situ by endogenous tissue transglutaminase. Eur J Immunol 2001; 31: 1317-23. 18. Mazzarella G, Maglio M, Paparo F, Tardone G, Stefanile R, Greco L, et al. An immunodominant DQ8-restricted gliadin peptide activates small intestinal immune response in in vitro cultured treated coeliac mucosa. J Pediatr Gastroenterol Nutr 2000; 31: S18. 19. de Waal Malefyt R, Haanen J, Spits H, Roncarlo MG, te Velde A, Figdor C, et al. Interleukin 10 (IL-10) and viral IL-10 strongly reduce antigen-specific human T cell proliferation by diminishing the antigen-presenting capacity of monocytes via downregulation of class-II major histocompatibilty complex expression. J Exp Med 1991; 174: 915-24. 20. Groux H, Bigler M, de Vries J, Roncarolo MG. Interleukin-10 induces a longterm antigen specific anergic state in human CD4+ T cells. J Exp Med 1996; 184: 19-29. 21. Salvati V, Troncone R, Mazzarella G, Stefanile R, Borrelli M, Riccio F, et al. Recombinant IL-10 down-regulates T-Cell activation and mRNA expression of proinflammatory cytokines in treated celiac mucosa in vitro cultured with gliadin. Scand J Immunol 2000; 4: 438 C25. 22. Myers LK, Seyer JM, Stuart JM, Kang AH. Suppression of murine collageninduced arthritis by nasal administration of collagen. Immunology 1997; 90: 161-4. 23. Rossi M, Maurano F, Caputo N, Auricchio S, Sette A, Capparelli R, et al. Intravenous or intranasal administration of gliadin is able to down-regulate the specific immune response in mice. Scand J Immunol 1999; 50: 177-82.
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 89-92 The most recent advances on gluten toxicity in coeliac disease 1 2 3 Gino Roberto Corazza , Carlo Catassi , Alessio Fasano 1 Department of Gastroenterology, University of Pavia, Italy; 2 Department of Pediatrics, University 3 of Ancona, Italy; Division of Pediatric Gastroenterology, Center for Celiac Research, University of Maryland, Baltimore, MD, USA After the Pavia meeting held on October 12, 2001, significant advances on the possibilities of a primary prevention of coeliac disease have been achieved. While a part of these have been recently published, most issues were discussed at the 10th International Symposium on Coeliac Disease held at the Pasteur Institute in Paris, last June. The majority of these works deals with a further characterization of the gluten peptides that trigger a T cell response. Although it is worth reminding that T cell activation does not always mirror gluten toxicity in vitro or in vivo, the reportoire of gluten peptides that are able to induce T cell activation seems now wider and more heterogenous than reported at the Pavia meeting. At that time two different groups found that a region of a-gliadin corresponding to aminoacids 57-75 acted as powerful, immunodominant epitope if a glutamine residue (Q65) was deamidated by tissue 1-2 transglutaminase (tTG) to glutamic acid . Those findings disclosed new exciting perspectives on possible alternatives for the treatment of coeliac disease, such as the achievement of a non-toxic wheat by removal or modification of the above mentioned antigenic sequences or specific immune therapy to induce oral tolerance. Looking at the T cell profile in coeliac children with recent onset of disease, 3 Koning's group found that 6 novel additional gliadin and glutenin peptides were able to induce T cell responses in the early phase of the pathogenesis of this condition. The observation that immune activation was at some extent independent of deamidation indicated that T cell responses can also be initiated by native gluten peptides. On the basis of their results they estimated that gluten may contain up to 50 T-cell antigenic peptide sequences (gliadin plus glutenin). No doubt that these results weakened the 4 expectations for new therapeutic approaches for this condition . In particular, as far as the production of genetically detoxified grains is concerned, to the technical difficulties listed by Biagi et al (pp 75-82 of this volume), the demonstration that glutenin peptides are able to induce T-cell activation in coeliac disease makes the suggestion of introducing high molecular weight glutenin genes to improve baking quality of maize no longer tenable. On the other side, the observation that the number of peptides 89
Page 1:
Perspectives on Coeliac Disease Vol
Page 4:
The AIC Meeting was held in the Aul
Page 8 and 9:
Italian Coeliac Society, Via Picott
Page 11 and 12:
Preface Coeliac disease (CD) is a u
Page 13:
Contents Current understanding of t
Page 16 and 17:
2 THE BASIS OF COELIAC DISEASE hapl
Page 18 and 19:
4 THE BASIS OF COELIAC DISEASE 1 pr
Page 20 and 21:
6 THE BASIS OF COELIAC DISEASE spre
Page 22 and 23:
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 34 and 35:
Page 36 and 37:
Page 38 and 39:
Page 40 and 41:
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 49 and 50:
COELIAC DISEASE IN THE SAHARAWI 35
Page 51 and 52: COELIAC DISEASE IN THE SAHARAWI 37
Page 53 and 54: COELIAC DISEASE IN THE SAHARAWI 39
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 89 and 90: Catassi C, Fasano A, Corazza GR (ed
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 97 and 98: Catassi C, Fasano A, Corazza GR (ed
Page 99 and 100: IMMUNOTHERAPY OF COELIAC DISEASE 85
Page 101: 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
show all

primary prevention of coeliac disease - Associazione Italiana ...

Create successful ePaper yourself

Delete template?

Save as template?