Mechanisms of gastric mucosal cell loss in autoimmune gastritis.
The causes of target cell death in organ-specific autoimmune diseases are not precisely known. In the case of EAG, parietal cell death depends on Th1 CD4 T cells and Fas/Fas-ligand, either through interaction between infiltrating CD4 T cells with gastric parietal cells that have upregulated Fas expression or through homotypic interactions between the parietal cells. TNF-alpha does not appear to have a role in this process. The accompanying loss of zymogenic cells is likely a consequence of the interruption of the normal developmental pathway in the gastric mucosa that follows the destruction of parietal cells in the gastric mucosa.
Marshall
Aiden C J
AC
Department of Pathology and Immunology, Monash University Medical School, Prahran, Victoria, Australia.
Alderuccio
Frank
F
Murphy
Kim
K
Toh
Ban-Hock
BH
D000818:Animals; D017209:Apoptosis; D001327:Autoimmune Diseases / Q000276:immunology* / Q000473:pathology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D016207:Cytokines / Q000502:physiology; D053222:Fas Ligand Protein; D005756:Gastritis / Q000276:immunology* / Q000473:pathology; D006801:Humans; D008562:Membrane Glycoproteins / Q000502:physiology*; D051379:Mice; D010295:Parietal Cells, Gastric / Q000276:immunology* / Q000473:pathology*; D018124:Receptors, Tumor Necrosis Factor / Q000502:physiology; D015398:Signal Transduction; D018417:Th1 Cells / Q000276:immunology
D016207:Cytokines; C505661:FASLG protein, human; D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D008562:Membrane Glycoproteins; D018124:Receptors, Tumor Necrosis Factor