125 - Autoimmune gastritis
Autor(s): A. Antico
Issue: RIMeL - IJLaM, Vol. 4, N. 2, 2008 (MAF Servizi srl ed.)
Page(s): 125-133
Autoimmune gastritis (AIG) is an organ specific disease characterised by atrophy of the corpus and fundus with sparing of the antrum, and presence of circulating autoantibodies to parietal cells (APCA) and to intrinsic factor (anti-IF), their secretory product. This chronic gastritis exhibits submucosal infiltration of mononuclear cells extending into the lamina propria between the gastric glands, with loss of parietal and zymogenic cells. The mononuclear cells are predominantly macrophages, B cells and CD4 T cells producing Th1-type cytokines. The CD4 T cells recognize parietal cell H+/K+-Adenosintriphosphatase (ATPase) and appear to be important in the pathogenesis of the gastritis, because transfer of these cells into naive mice results in gastritis and production of serum autoantibodies to gastric H+/K+-ATPase. Regardless of whether APCA and anti-IF are pathogenic or not, their presence provide a convenient diagnostic probe for autoimmune atrophic gastritis. The immunologic mechanisms that allow the initiation and progression of the T cell response leading to autoimmune gastritis remain to be established. Parietal cells release ATPase during normal cell turnover, which may result in its selective uptake and processing by antigen-presenting cells, alternatively Helicobacter pylori infection may play an initiating role in the pathogenesis of AIG. Chronic autoaggression to the gastric proton pump may result in decreased gastric acid secretion, hypergastrinaem