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CD4 + T cells, but not CD8 + T cells, are required for the development of experimental autoimmune gastritis
Author(s) -
H D De Silva,
Ian R. van Driel,
Nicole L. La Gruta,
BanHock Toh,
Paul A. Gleeson
Publication year - 1998
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1998.00436.x
Subject(s) - autoimmune gastritis , cd8 , autoantibody , gastritis , antibody , biology , cytotoxic t cell , immunology , stomach , microbiology and biotechnology , antigen , pathology , medicine , autoimmunity , in vitro , biochemistry
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.