1887

Chapter 36 : Gastric Autoimmunity

MyBook is a cheap paperback edition of the original book and will be sold at uniform, low price.

Ebook: Choose a downloadable PDF or ePub file. Chapter is a downloadable PDF file. File must be downloaded within 48 hours of purchase

Buy this Chapter
Digital (?) $15.00

Preview this chapter:
Zoom in
Zoomout

Gastric Autoimmunity, Page 1 of 2

| /docserver/preview/fulltext/10.1128/9781555818005/9781555812133_Chap36-1.gif /docserver/preview/fulltext/10.1128/9781555818005/9781555812133_Chap36-2.gif

Abstract:

This chapter describes the antigastric antibody responses to infection in humans. Particular types of antibodies, those directed against parietal cell canaliculi, are likely to be clinically relevant in -associated antigastric autoimmunity. Second, the pathogenesis of classical autoimmune gastritis and pernicious anemia (AIG/PA) and the pathogenesis of -associated atrophic gastritis are reviewed. Through conventional histomorphological parameters of chronic gastritis such as grade, activity, and distribution of gastritis, as well as the presence of glandular atrophy and intestinal metaplasia, it has been found that gastritis in the corpus mucosa was more severe in patients with anticanalicular autoantibodies than in patients without these types of autoantibodies. In both histopathological and clinical characteristics, -induced gastritis with anticanalicular antibodies and corpus atrophy resembles to some extent classical AIG/PA. A number of studies indicate that a substantial portion of patients with autoimmune gastritis have or have had infection. Adoptive transfer of mononuclear cells from gastritic mice have shown that experimental murine autoimmune gastritis (EAIG), induced either by immunization with the gastric H,K-ATPase or by neonatal thymectomy, is mediated by CD4, but not CD8, T cells. T cell precursors, expressing neither the TCR nor the two coreceptors, CD4 and CD8, migrate from the bone marrow to the thymus. The cytokine "milieu," present during the first encounter of naive T helper cells with their specific immunogenic peptides, plays an important role in development of EAIG.

Citation: Bergman M, Vandenbroucke-Grauls C, Appelmelk B, Faller G, D'Elios M, Del Prete G. 2001. Gastric Autoimmunity, p 429-440. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch36

Key Concept Ranking

T Helper Cells
0.5337557
MHC Class II
0.50433975
Major Histocompatibility Complex
0.49841833
Tumor Necrosis Factor
0.46663216
0.5337557
Highlighted Text: Show | Hide
Loading full text...

Full text loading...

Figures

Image of Figure 1
Figure 1

(A) Immunoreactivity of anticanalicular autoantibodies on canalicular membranes within parietal cells of the human gastric corpus mucosa (by immunohistochemistry; original magnification × 20). pylori-infected patient serum reacts with a section from the glandular region of the corpus of an uninfected person. (B) Staining of parietal cells in detail (original magnification × 100). The black structures are parietal cell canaliculi containing the predominant canalicular antigen, i.e., gastric H,K-ATPase, and which are stained by the pylon-induced autoantibodies to H, K-ATPase.

Citation: Bergman M, Vandenbroucke-Grauls C, Appelmelk B, Faller G, D'Elios M, Del Prete G. 2001. Gastric Autoimmunity, p 429-440. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch36
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 2
Figure 2

A model of the pathogenesis in atrophic corpus gastritis. infection leads to an inflammatory influx of T and B lymphocytes and macrophages, results in a predominant Th1 cytokine milieu in the gastric mucosa, and induces aberrant MHC class II expression on gastric epithelial cells. Gastric epithelial cells (including parietal cells) acquire the phenotype of APCs as result of IFN-γ- and TNF-α-induced expression of b7.2 costimulatory molecules and start to express Fas. Parietal cells may be killed by t cells by the following mechanisms (panels A to D): (A) Parietal cells presenting gastric H,K-ATPase may activate autoreactive H,K-ATPase-specific CD4 t cells that have escaped negative selection in the thymus, and may subsequently be killed by Fas-FasL-mediated apoptosis. (B) H,K-ATPase-specific t cells may also be activated by professional APCs, such as dendritic cells (DC), and kill H,K-ATPase-presenting parietal cells by Fas-FasL interaction. (C) Activated CD4 T cells may kill Fas-expressing parietal cells by Fas-FasL-mediated bystander lysis, irrespective of the antigen that is presented by the parietal cell. (D) Parietal cells could present leakage-derived antigens to H. pylori-specific T cells and may subsequently be killed by Fas-FasL-mediated apoptosis. Additionally, t cells may be activated by professional APCs.

Citation: Bergman M, Vandenbroucke-Grauls C, Appelmelk B, Faller G, D'Elios M, Del Prete G. 2001. Gastric Autoimmunity, p 429-440. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch36
Permissions and Reprints Request Permissions
Download as Powerpoint

References

/content/book/10.1128/9781555818005.chap36
1. Alderuccio, F.,, P. A. Gleeson,, S. P. Berzins,, M. Martin,, I. R. van Driel,, and B. H. Toh. 1997. Expression of the gastric H/K-ATPase alpha-subunit in the thymus may explain the dominant role of the beta-subunit in the pathogenesis of autoimmune gastritis. Autoimmunity 25:167175.
2. Alderuccio, F.,, and B. H. Toh. 1998. Spontaneous autoimmune gastritis in C3H/He mice: a new mouse model for gastric autoimmunity. Am. J. Pathol. 153:13111318.
3. Alderuccio, F.,, B. H. Toh,, P. A. Gleeson,, and I. R. van Driel. 1995. A novel method for isolating mononuclear cells from the stomachs of mice with experimental autoimmune gastritis. Autoimmunity 21:215221.
4. Alderuccio, F.,, B. H. Toh,, S. S. Tan,, P. A. Gleeson,, and I. R. van Driel. 1993. An autoimmune disease with multiple molecular targets abrogated by the transgenic expression of a single autoantigen in the thymus. J. Exp. Med. 178:419426.
5. Appelmelk, B. J.,, G. Faller,, D. Claeys,, T. Kirchner,, and C. M. J. E Vandenbroucke-Grauls. 1998. Bugs on trial: the case of Helicobacter pylori and autoimmunity. Immunol. Today 19: 296299.
6. Archimandritis, A.,, S. Sougioultzis,, P. G. Foukas,, M. Tzivras,, P. Davaris,, and H. M. Moutsopoulos. 2000. Expression of HLA-DR, costimulatory molecules B7-1, B7-2, intercellular adhesion molecule-1 (ICAM-1) and Fas ligand (FasL) on gastric epithelial cells in Helicobacter pylori gastritis; influence of H. pylori eradication. Clin. Exp. Immunol. 119:464471.
7. Ardill, J. E.,, C. J. Larkin,, D. Fillmore,, and K. D. Buchanan. 1998. Autoantibodies to gastrin in patients with pernicious anaemia: a novel antibody. Q. J. Med. 91:739742.
8. Bamford, K. B.,, X. Fan,, S. E. Crowe,, J. F. Leary,, W. K. Gourley,, G. K. Luthra,, E. G. Brooks,, D. Y. Graham,, V. E. Reyes,, and P. B. Ernst. 1998. Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 pheno-type. Gastroenterology 114:482492.
9. Barrett, S. P.,, P. A. Gleeson,, H. de Silva,, B. H. Toh,, and I. R. van Driel. 1996. Interferon-gamma is required during the initiation of an organ-specific autoimmune disease. Eur. J. Immunol. 26:16521655.
10. Barrett, S. P.,, A. Riordon,, B. H. Toh,, P. A. Gleeson,, and I. R. van Driel. 2000. Homing and adhesion molecules in autoimmune gastritis. J. Leukoc. Biol. 67:169173.
11. Barrett, S. P.,, B. H. Toh,, F. Alderuccio,, I. R. van Driel,, and P. A. Gleeson. 1995. Organ-specific autoimmunity induced by adult thymectomy and cyclophosphamide-induced lymphopenia. Eur. J. Immunol. 25:238244.
12. Burman, P.,, O. Kampe,, W. Kraaz,, L. Loof,, A. Smolka,, A. Karlsson,, and A. Karlsson-Parra. 1992. A study of autoimmune gastritis in the postpartum period and at a 5-year follow-up. Gastroenterology 103:934942.
13. Callaghan, J. M.,, M. A. Khan,, F. Alderuccio,, I. R. van Driel,, P. A. Gleeson,, and B. H. Toh. 1993. Alpha and beta subunits of the gastric H + /K( + )-ATPase are concordantly targeted by parietal cell autoantibodies associated with autoimmune gastritis. Autoimmunity 16:289295.
14. Cappell, M. S.,, and A. Garcia. 1998. Gastric and duodenal ulcers during pregnancy. Gastroenterol. Clin. North Am. 27: 169195.
15. Claeys, D.,, G. Faller,, B. J. Appelmelk,, R. Negrini,, and T. Kirchner. 1998. The gastric H + ,K +-ATPase is a major autoantigen in chronic Helicobacter pylori gastritis with body mucosa atrophy. Gastroenterology 115:340347.
16. Claeys, D.,, E. Saraga,, B. C. Rossier,, and J. P. Kraehenbuhl. 1997. Neonatal injection of native proton pump antigens induces autoimmune gastritis in mice. Gastroenterology 113: 11361145.
17. D'Elios, M. M.,, L. P. Andersen,, and G. Del Prete. 1998. Inflammation and host response. Curr. Opin. Gastroenterol. 14: 1519.
18. D'Elios, M. M.,, M. Manghetti,, F. Almerigogna,, A. Amedei,, F. Costa,, D. Burroni,, C. T. Baldari,, S. Romagnani,, J. L. Telford,, and G. Del Prete. 1997. Different cytokine profile and antigen-specificity repertoire in Helicobacter pylori-specific T cell clones from the antrum of chronic gastritis patients with or without peptic ulcer. Eur. J. Immunol. 27:17511755.
19. D'Elios, M. M.,, M. Manghetti,, M. De Carli,, F. Costa,, C. T. Baldari,, D. Burroni,, J. L. Telford,, S. Romagnani,, and G. Del Prete. 1997. T helper 1 effector cells specific for Helicobacter pylori in the gastric antrum of patients with peptic ulcer disease. J. Immunol. 158:962967.
20. Del Prete, G. F.,, M. De Carli,, C. Mastromauro,, R. Biagiotti,, D. Macchia,, P. Falagiani,, M. Ricci,, and S. Romagnani. 1991. Purified protein derivative of Mycobacterium tuberculosis and excretory-secretory antigen(s) of Toxocara canis expand in vitro human T cells with stable and opposite (type 1 T helper or type 2 T helper) profile of cytokine production. J. Clin. Invest. 88:346350.
21. De Silva, H. D.,, P. A. Gleeson,, B. H. Toh,, I. R. van Driel,, and F. R. Carbone. 1999. Identification of a gastritogenic epitope of the H/K ATPase beta-subunit. Immunology 96:145151.
22. De Silva, H. D.,, I. R. van Driel,, N. La Grata,, B. H. Toh,, and P. A. Gleeson. 1998. CD4+ T cells, but not CD8+ T cells, are required for the development of experimental autoimmune gastritis. Immunology 93:405408.
23. Eaton, K. A.,, S. R. Ringler,, and S. J. Danon. 1999. Murine splenocytes induce severe gastritis and delayed-type hypersensitivity and suppress bacterial colonization in Helicobacter pylori-infected SCID mice. Infect. Immun. 67:45944602.
24. Eidt, S.,, G. Oberhuber,, A. Schneider,, and M. Stolte. 1996. The histopathological spectrum of type A gastritis. Pathol. Res. Pract. 192:101106.
25. Engstrand, L.,, A. Scheynius,, C. Pahlson,, L. Grimelius,, A. Schwan,, and S. Gustavsson. 1989. Association of Campylobacter pylori with induced expression of class II transplantation antigens on gastric epithelial cells. Infect. Immun. 57: 827832.
26. Faller, G.,, and T. Kirchner. 2000. Role of antigastric autoantibodies in chronic Helicobacter pylori infection. Microsc. Res. Tech. 48:321326.
27. Faller, G.,, H. Steininger,, M. Eck,, J. Hensen,, E. G. Hann,, and T. Kirchner. 1996. Antigastric autoantibodies in Helicobacter pylori gastritis: prevalence, in-situ binding sites and clues for clinical relevance. Virchows Arch. 427:483486.
28. Faller, G.,, H. Steininger,, J. Kränzlein,, H. Maul,, T. Kerkau,, J. Hensen,, E. G. Hahn,, and T. Kirchner. 1997. Antigastric autoantibodies in Helicobacter pylori infection: implications of histological and clinical parameters of gastritis. Gut 41: 619623.
29. Faller, G.,, M. Winter,, H. Steininger,, P. Konturek,, S. J. Kont-urek,, and T. Kirchner. 1998. Antigastric autoantibodies and gastric secretory function in Helicobacter pylori-infected patients with duodenal ulcer and non-ulcer dyspepsia. Scand. J. Gastroenterol. 33:276282.
30. Faller, G.,, M. Winter,, H. Steininger,, N. Lehn,, A. Meining,, E. Bayerdorffer,, and T. Kirchner. 1999. Decrease of antigastric autoantibodies in Helicobacter pylori gastritis after cure of infection. Pathol. Res. Pract. 195:243246.
31. Fan, X.,, S. E. Crowe,, S. Behar,, H. Gunasena,, G. Ye,, H. Haeberle,, N. van Houten,, W. K. Gourley,, P. B. Ernst,, and V. E. Reyes. 1998. The effect of class II major histocompatibility complex expression on adherence of Helicobacter pylori and induction of apoptosis in gastric epithelial cells: a mechanism for T helper cell type 1-mediated damage. J. Exp. Med. 187: 16591669.
32. Fox, J. G.,, P. Beck,, C. A. Dangler,, M. T. Whary,, T. C. Wang,, H. N. Shi,, and C. Nagler-Anderson. 2000. Concurrent enteric helminth infection modulates inflammation and gastric immune responses and reduces helicobacter-induced gastric atrophy. Nat. Med. 6:536542.
33. Fukuma, K.,, S. Sakaguchi,, K. Kuribayashi,, W. L. Chen,, R. Morishita,, K. Sekita,, H. Uchino,, and T. Masuda. 1988. Immunologic and clinical studies on murine experimental autoimmune gastritis induced by neonatal thymectomy. Gastroenterology 94:274283.
34. Gleeson, P. A.,, and B. H. Toh. 1991. Molecular targets in pernicious anaemia. Immunol. Today 12:233238.
35. Gleeson, P. A.,, B. H. Toh,, and I. R. van Driel. 1996. Organ-specific autoimmunity induced by lymphopenia. Immunol. Rev. 149:97125.
36. Goldkorn, I.,, P. A. Gleeson,, and B. H. Toh. 1989. Gastric parietal cell antigens of 60-90, 92, and 100-120 kDa associated with autoimmune gastritis and pernicious anemia. Role of N-glycans in the structure and antigenicity of the 60-90-kDa component. J. Biol. Chem. 264:1876818774.
37. Holcombe, C. 1992. Helicobacter pylori: the African enigma. Gut 33:429431.
38. Hruby, Z.,, K. Myszka-Bijak,, G. Gosciniak,, J. Blaszczuk,, Czyz, W.,, P. Kowalski,, K. Falkiewicz,, G. Szymanska,, and A. Przondo-Mordarska. 1997. Helicobacter pylori in kidney allograft recipients: high prevalence of colonization and low incidence of active inflammatory lesions. Nephron 75:2529.
39. Jones, C. M.,, J. M. Callaghan,, P. A. Gleeson,, Y. Mori,, T. Masuda,, and B. H. Toh. 1991. The parietal cell autoantigens recognized in neonatal thymectomy-induced murine gastritis are the alpha and beta subunits of the gastric proton pump. Gastroenterology 101:287294.
40. Karlsson, F. A.,, P. Burman,, L. Loof,, and S. Mardh. 1988. Major parietal cell antigen in autoimmune gastritis with pernicious anemia is the acid-producing H + ,K +-adenosine triphosphatase of the stomach. J. Clin. Invest. 81:475479.
41. Karnes, W. E., Jr.,, I. M. Samloff,, M. Siurala,, M. Kekki,, P. Sipponen,, S. W. Kim,, and J. H. Walsh. 1991. Positive serum antibody and negative tissue staining for Helicobacter pylori in subjects with atrophic body gastritis. Gastroenterology 101: 167174.
42. Kojima, A.,, O. Taguchi,, and Y. Nishizuka. 1980. Experimental production of possible autoimmune castritis followed by macrocytic anemia in athymic nude mice. Lab. Invest. 42: 387395.
43. Kuipers, E. J. 1997. Helicobacter pylori and the risk and management of associated diseases: gastritis, ulcer disease, atrophic gastritis and gastric cancer. Aliment. Pharmacol. Ther. 11(Suppl. l):7188.
44. Ma, J. Y.,, K. Borch,, S. E. Sjöstrand,, L. Janzon,, and S. Mardh. 1994. Positive correlation between H,K-adenosine triphosphatase autoantibodies and Helicobacter pylori antibodies in patients with pernicious anemia. Scand. J. Gastroenterol. 29: 961965.
45. Maor-Kendler, Y.,, G. Gabay,, J. Bernheim,, T. Naftali,, I. Lesin,, G. Leichtman,, I. Pomeranz,, and B. Novis. 1999. Expression of bcl-2 in autoimmune and Helicobacter pylori-associated atrophic gastritis. Dig. Dis. Sci. 44:680685.
46. Mardh, S.,, J. Y. Ma,, Y. H. Song,, A. Aly,, and K. Henriksson. 1991. Occurrence of autoantibodies against intrinsic factor, H,K-ATPase, and pepsinogen in atrophic gastritis and rheumatoid arthritis. Scand. J. Gastroenterol. 26:10891096.
47. Mardh, S.,, and Y. H. Song. 1989. Characterization of antigenic structures in autoimmune atrophic gastritis with pernicious anaemia. The parietal cell H,K-ATPase and the chief cell pepsinogen are the two major antigens. Acta Physiol. Scand. 136: 581587.
48. Martinelli, T. M.,, I. R. van Driel,, F. Alderuccio,, P. A. Gleeson,, and B. H. Toh. 1996. Analysis of mononuclear cell infiltrate and cytokine production in murine autoimmune gastritis. Gastroenterology 110:17911802.
49. Mohammadi, M.,, S. Czinn,, R. Redline,, and J. Nedrud. 1996. Helicobacter-specific cell-mediated immune responses display a predominant Th1 phenotype and promote a delayed-type hypersensitivity response in the stomachs of mice. J. Immunol. 156:47294738.
50. Mohammadi, M.,, J. Nedrud,, R. Redline,, N. Lycke,, and S. J. Czinn. 1997. Murine CD4 T-cell response to Helicobacter infection: TH1 cells enhance gastritis and TH2 cells reduce bacterial load. Gastroenterology 113:18481857.
51. Mori, Y.,, K. Fukuma,, Y. Adachi,, K. Shigeta,, R. Kannagi,, H. Tanaka,, M. Sakai,, K. Kuribayashi,, H. Uchino,, and T. Masuda. 1989. Parietal cell autoantigens involved in neonatal thymectomy-induced murine autoimmune gastritis. Studies using monoclonal autoantibodies. Gastroenterology 97: 364375.
52. Negrini, R.,, L. Lisato,, I. Zanella,, L. Cavazzini,, S. Gullini,, V. Villanacci,, C. Poiesi,, A. Albertini,, and S. Ghielmi. 1991. Helicobacter pylori infection induces antibodies cross-reacting with human gastric mucosa. Gastroenterology 101:437445.
53. Negrini, R.,, A. Savio,, C. Poiesi,, B. J. Appelmelk,, F. Buffoli,, A. Paterlini,, P. Cesari,, M. Graffeo,, D. Vaira,, and G. Franzin. 1996. Antigenic mimicry between Helicobacter pylori and gastric mucosa in the pathogenesis of body atrophic gastritis. Gastroenterology 111:655665.
54. Nishio, A.,, M. Hosono,, Y. Watanabe,, M. Sakai,, M. Okuma,, and T. Masuda. 1994. A conserved epitope on H + ,K( + )-adenosine triphosphatase of parietal cells discerned by a murine gastritogenic T-cell clone. Gastroenterology 107: 14081414.
55. Nishio, A.,, T. Katakai,, C. Oshima,, S. Kasakura,, M. Sakai,, S. Yonehara,, T. Suda,, S. Nagata,, and T. Masuda. 1996. A possible involvement of Fas-Fas ligand signaling in the pathogenesis of murine autoimmune gastritis. Gastroenterology 111: 959967.
56. Parente, F.,, R. Negrini,, V. Imbesi,, G. Maconi,, C. Cucino,, and G. Bianchi Porro. 1999. The presence of gastric autoantibodies impairs gastric secretory function in patients with H. pylori-positive duodenal ulcer. Gut 45:A40.
57. Perez-Perez, G. I. 1997. Role of Helicobacter pylori infection in the development of pernicious anemia. Clin. Infect. Dis. 25: 10201022.
58. Ramsdell, F.,, M. S. Seaman,, R. E. Miller,, K. S. Picha,, M. K. Kennedy,, and D. H. Lynch. 1994. Differential ability of Th1 and Th2 T cells to express Fas ligand and to undergo activation-induced cell death. Int. Immunol. 6:15451553.
59. Romagnani, S.,, P. Parronchi,, M. M. D'Elios,, P. Romagnani,, F. Annunziato,, M. P. Piccinni,, R. Manetti,, S. Sampognaro,, C. Mavilia,, M. De Carli,, E. Maggi,, and G. F. Del Prete. 1997. An update on human Th1 and Th2 cells. Int. Arch. Allergy Immunol. 113:153156.
60. Roth, K. A.,, S. B. Kapadia,, S. M. Martin,, and R. G. Lorenz. 1999. Cellular immune responses are essential for the development of Helicobacter felis-associated gastric pathology. J. Immunol. 163:14901497.
61. Sabelko-Downes, K. A.,, and J. H. Russell. 2000. The role of fas ligand in vivo as a cause and regulator of pathogenesis. Curr. Opin. Immunol. 12:330335.
62. Sakagami, T.,, M. Dixon,, J. O'Rourke,, R. Howlett,, F. Alderuccio,, J. Vella,, T. Shimoyama,, and A. Lee. 1996. Atrophic gastric changes in both Helicobacter felis and Helicobacter pylori infected mice are host dependent and separate from antral gastritis. Gut 39:639648.
63. Sakaguchi, S.,, T. H. Ermak,, M. Toda,, L. J. Berg,, W. Ho,, D. S. Fazekas,, P. A. Peterson,, N. Sakaguchi,, and M. M. Davis. 1994. Induction of autoimmune disease in mice by germline alteration of the T cell receptor gene expression. J. Immunol. 152:14711484.
64. Scarff, K. J.,, J. M. Pettitt,, I. R. van Driel,, P. A. Gleeson,, and B. H. Toh. 1997. Immunization with gastric H+/K( + )-ATPase induces a reversible autoimmune gastritis. Immunology 92: 9198.
65. Shirin, H.,, and S. F. Moss. 1998. Helicobacter pylori induced apoptosis. Gut 43:592594.
66. Steininger, H.,, E. Dewald,, G. Faller,, and T. Kirchner. 1996. Rate of apoptosis in chronic gastritis and correlation with antigastric autoantibodies. Gut 39:A262.
67. Steininger, H.,, G. Faller,, E. Dewald,, T. Brabletz,, A. Jung,, and T. Kirchner. 1998. Apoptosis in chronic gastritis and its correlation with antigastric autoantibodies. Virchows Arch. 433: 1318.
68. Stolte, M.,, K. Baumann,, B. Bethke,, M. Ritter,, E. Lauer,, and H. Eidt. 1992. Active autoimmune gastritis without total atrophy of the glands. Z. Gastroenterol. 30:729735.
69. Stolte, M.,, E. Meier,, and A. Meining. 1998. Cure of autoimmune gastritis by Helicobacter pylori eradication in a 21-year-old male. Z. Gastroenterol. 36:641643.
70. Suri-Payer, E.,, A. Z. Amar,, R. McHugh,, K. Natarajan,, D. H. Margulies,, and E. M. Shevach. 1999. Post-thymectomy autoimmune gastritis: fine specificity and pathogenicity of anti-H/ K ATPase-reactive T cells. Eur. J. Immunol. 29:669677.
71. Suri-Payer, E.,, P. J. Kehn,, A. W. Cheever,, and E. M. Shevach. 1996. Pathogenesis of post-thymectomy autoimmune gastritis. Identification of anti-H/K adenosine triphosphatase-reactive T cells. J. Immunol. 157:17991805.
72. Toh, B. H.,, P. A. Gleeson,, R. J. Simpson,, R. L. Moritz,, J. M. Callaghan,, I. Goldkorn,, C. M. Jones,, T. M. Martinelli,, F. T. Mu,, and D. C. Humphris. 1990. The 60- to 90-kDa parietal cell autoantigen associated with autoimmune gastritis is a beta subunit of the gastric H + /K( + )-ATPase (proton pump). Proc. Natl. Acad. Sci. USA 87:64186422.
73. Toh, B. H.,, J. W. Sentry,, and F. Alderuccio. 2000. The causative H + /K+ ATPase antigen in the pathogenesis of autoimmune gastritis. Immunol. Today 21:348354.
74. Toh, B. H.,, I. R. van Driel,, and P. A. Gleeson. 1997. Pernicious anemia. N. Engl. J. Med. 337:14411448.
75. Tucci, A.,, L. Poli,, C. Tosetti,, G. Biasco,, W. Grigioni,, O. Varoli,, C. Mazzoni,, G. F. Paparo,, V. Stanghellini,, and G. Caletti. 1998. Reversal of fundic atrophy after eradication of Helicobacter pylori. Am. J. Gastroenterol. 93:14251431.
76. Valle, J.,, M. Kekki,, P. Sipponen,, T. Ihamäki,, and M. Siurala. 1996. Long-term course and consequences of Helicobacter pylori gastritis. Results of a 32-year follow-up study. Scand. J. Gastroenterol. 31:546550.
77. Vorobjova, T.,, G. Faller,, H. I. Maaroos,, P. Sipponen,, K. Villako,, R. Uibo,, and T. Kirchner. 2000. Significant increase in antigastric autoantibodies in a long-term follow-up study of H. pylori gastritis. Virchows Arch. 437:3745.
78. Wang, J.,, X. Fan,, C. Lindholm,, M. Bennett,, J. O'Connoll,, F. Shanahan,, E. G. Brooks,, V. E. Reyes,, and P. B. Ernst. 2000. Helicobacter pylori modulates lymphoepithelial cell interactions leading to epithelial cell damage through Fas/Fas ligand interactions. Infect. Immun. 68:43034311.
79. Ye, G.,, C. Barrera,, X. Fan,, W. K. Gourley,, S. E. Crowe,, P. B. Ernst,, and V. E. Reyes. 1997. Expression of B7-1 and B7-2 costimulatory molecules by human gastric epithelial cells: potential role in CD4 + T cell activation during Helicobacter pylori infection. J. Clin. Invest. 99:16281636.

Tables

Generic image for table
Table 1

Evidence for the clinical relevance of antigastric autoimmmunity in gastritis

Citation: Bergman M, Vandenbroucke-Grauls C, Appelmelk B, Faller G, D'Elios M, Del Prete G. 2001. Gastric Autoimmunity, p 429-440. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch36

This is a required field
Please enter a valid email address
Please check the format of the address you have entered.
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error