Chapter 36 : Gastric Autoimmunity

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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
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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
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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
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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

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