Mouse mammary tumor virus superantigens and murine autoimmune gastritis

Gastroenterology. 1994 Oct;107(4):924-33. doi: 10.1016/0016-5085(94)90215-1.

Abstract

Background/aims: Neonatal thymectomy induces autoimmune gastritis in BALB/c (minor lymphocyte-stimulating antigen [Mls]-1b) mice, whereas DBA/2 (Mls-1a) mice are resistant. Resistance has been linked to the Mls-1a locus, which encodes a retroviral superantigen, and to superantigen reactive T cells that express V beta 6+ T-cell receptors. V beta 6+ T cells are known to be deleted in mice expressing Mls-1a superantigens.

Methods: Neonatal thymectomized BALB/c and Mls-1a congenic BALB.D2.Mls-1a mice were analyzed to examine directly the role of Mls-1a self-superantigens and V beta 6+ T cells in autoimmune gastritis.

Results: Autoimmune gastritis was detected in thymectomized BALB.D2.Mls-1a mice with high incidence. Autoantibodies to the gastric H+,K(+)-adenosine triphosphatase were present independent of the Mls phenotype in sera of gastritic mice. Severe gastritis had already appeared 1 month after thymectomy in BALB.D2.Mls-1a mice. V beta 6+ T cells were deleted in the stomach lymph nodes of 1-month-old gastritic BALB.D2.Mls-1a mice but could be detected by immunocytochemistry in the stomach lesions.

Conclusions: Endogenous Mls-1a self-superantigens and Mls-1a reactive V beta 6+ T cells are not involved in resistance to autoimmune gastritis in BALB.D2 mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Autoimmune Diseases / immunology*
  • CD4-Positive T-Lymphocytes / metabolism
  • CD4-Positive T-Lymphocytes / physiology
  • Disease Susceptibility
  • Gastritis / immunology*
  • Gastritis / pathology
  • Mammary Tumor Virus, Mouse / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Receptors, Antigen, T-Cell / metabolism
  • Superantigens / immunology*
  • Thymectomy

Substances

  • Receptors, Antigen, T-Cell
  • Superantigens