CD4+ T cells, but not CD8+ T cells, are required for the development of experimental autoimmune gastritis

• Published in: Immunology Vol. 93; no. 3; pp. 405 - 408
• Main Authors: De Silva, H D, Van Driel, I R, La Gruta, N, Toh, B H, Gleeson, P A
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.03.1998
• Subjects: AIDS/HIV; Animals; Antibodies, Monoclonal - pharmacology; Autoimmune Diseases - immunology; CD4-Positive T-Lymphocytes - immunology; CD8-Positive T-Lymphocytes - immunology; Disease Models, Animal; Gastritis - immunology; Immunoglobulin G - immunology; Immunohistochemistry; Lymphocyte Depletion; Mice; Mice, Inbred BALB C; Thymectomy
• ISSN: 0019-2805; 1365-2567
• DOI: 10.1046/j.1365-2567.1998.00436.x

Murine autoimmune gastritis, induced by neonatal thymectomy, is characterized by a mononuclear infiltrate within the gastric mucosa, loss of parietal and zymogenic cells and circulating autoantibodies to the gastric H/K ATPase. The infiltrate contains both CD4+ and CD8+ T cells. Here we have investigated the roles of CD4+ and CD8+ T cells in the development of gastritis by in vivo treatment with depleting rat anti‐CD4 and anti‐CD8 monoclonal antibodies. Depletion of CD4+ T cells decreased the incidence of gastric mononuclear infiltrates from 63% (5/8), observed in normal rat immunoglobulin G (IgG)‐injected mice, to 8% (1/12) and also abolished the production of antigastric autoantibodies. In contrast, depletion of CD8+ T cells did not reduce the incidence of gastritis. The absence of CD8+ T cells in the infiltrate of the stomach of anti‐CD8+‐treated mice was confirmed by immunocytochemistry. These results argue that neonatal thymectomy‐induced autoimmune gastritis is mediated by CD4+ T cells and that CD8+ T cells do not play a significant role in the development of the gastric lesion.