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Experimental autoimmune gastritis: mouse models of human organ-specific autoimmune disease.
Int Rev Immunol 2005 Jan-Apr; 24(1-2):93-110IR

Abstract

Experimental autoimmune gastritis (EAG) is an excellent model of human autoimmune gastritis, the underlying cause of pernicious anaemia. Murine autoimmune gastritis replicates human gastritis in being characterized by a chronic inflammatory mononuclear cell infiltrate in the gastric mucosa, destruction of parietal and zymogenic cells, and autoantibodies to the alpha-and beta-subunits of the gastric H+/K+ ATPase. Disease is induced strain specifically in gastritis-susceptible BALB/c mice by methods with a greater variety than those for most other experimental autoimmune diseases. The disease is induced in the regional gastric lymph node in which pathogenic CD4+ T cells are recruited. The model provides an excellent illustration of regulation by CD4+CD25+T cells, and, indeed, the removal of such regulatory cells, e.g., by neonatal thymectomy, is thought to be a major mechanism by which disease can develop. The culprit T helper type 1 (Th1) CD4+ T cells recognize either the alpha- or beta-subunits of the gastric H+/K+ ATPase, but the beta-subunit appears to be the initiating autoantigen, while the alpha-subunit may have a role in perpetuating disease. Since no specific environmental modifiers are identifiable, the origins of the disease are intrinsic; this is illustrated by the capacity of a cytokine (GM-CSF)-dependent inflammatory stimulus in the stomach to initiate EAG, according to a transgenic model in which thymectomy is dispensible. Thus, EAG is an exquisite model for a reductionist analysis of the multiple elements that in combination induce autoimmunity in humans.

Authors+Show Affiliations

Department of Pathology and Immunology, Monash University Medical School, Prahran, Victoria, Australia.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

15763991

Citation

Field, J, et al. "Experimental Autoimmune Gastritis: Mouse Models of Human Organ-specific Autoimmune Disease." International Reviews of Immunology, vol. 24, no. 1-2, 2005, pp. 93-110.
Field J, Biondo MA, Murphy K, et al. Experimental autoimmune gastritis: mouse models of human organ-specific autoimmune disease. Int Rev Immunol. 2005;24(1-2):93-110.
Field, J., Biondo, M. A., Murphy, K., Alderuccio, F., & Toh, B. H. (2005). Experimental autoimmune gastritis: mouse models of human organ-specific autoimmune disease. International Reviews of Immunology, 24(1-2), pp. 93-110.
Field J, et al. Experimental Autoimmune Gastritis: Mouse Models of Human Organ-specific Autoimmune Disease. Int Rev Immunol. 2005;24(1-2):93-110. PubMed PMID: 15763991.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Experimental autoimmune gastritis: mouse models of human organ-specific autoimmune disease. AU - Field,J, AU - Biondo,M A, AU - Murphy,K, AU - Alderuccio,F, AU - Toh,B-H, PY - 2005/3/15/pubmed PY - 2005/5/6/medline PY - 2005/3/15/entrez SP - 93 EP - 110 JF - International reviews of immunology JO - Int. Rev. Immunol. VL - 24 IS - 1-2 N2 - Experimental autoimmune gastritis (EAG) is an excellent model of human autoimmune gastritis, the underlying cause of pernicious anaemia. Murine autoimmune gastritis replicates human gastritis in being characterized by a chronic inflammatory mononuclear cell infiltrate in the gastric mucosa, destruction of parietal and zymogenic cells, and autoantibodies to the alpha-and beta-subunits of the gastric H+/K+ ATPase. Disease is induced strain specifically in gastritis-susceptible BALB/c mice by methods with a greater variety than those for most other experimental autoimmune diseases. The disease is induced in the regional gastric lymph node in which pathogenic CD4+ T cells are recruited. The model provides an excellent illustration of regulation by CD4+CD25+T cells, and, indeed, the removal of such regulatory cells, e.g., by neonatal thymectomy, is thought to be a major mechanism by which disease can develop. The culprit T helper type 1 (Th1) CD4+ T cells recognize either the alpha- or beta-subunits of the gastric H+/K+ ATPase, but the beta-subunit appears to be the initiating autoantigen, while the alpha-subunit may have a role in perpetuating disease. Since no specific environmental modifiers are identifiable, the origins of the disease are intrinsic; this is illustrated by the capacity of a cytokine (GM-CSF)-dependent inflammatory stimulus in the stomach to initiate EAG, according to a transgenic model in which thymectomy is dispensible. Thus, EAG is an exquisite model for a reductionist analysis of the multiple elements that in combination induce autoimmunity in humans. SN - 0883-0185 UR - https://www.unboundmedicine.com/medline/citation/15763991/Experimental_autoimmune_gastritis:_mouse_models_of_human_organ_specific_autoimmune_disease_ L2 - http://www.tandfonline.com/doi/full/10.1080/08830180590884585 DB - PRIME DP - Unbound Medicine ER -