MOUSE MAMMARY-TUMOR VIRUS SUPERANTIGENS AND MURINE AUTOIMMUNE GASTRITIS

Background/Aims: Neonatal thymectomy induces autoimmune gastritis in BALB/c (minor lymphocyte-stimulating antigen [Mls]-1(b)) mice, whereas DBA/2 (Mls-1(a)) mice are resistant. Resistance has been linked to the Mls-1(a) 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-1(a) superantigens. Methods: Neonatal thymectomized BALB/c and Mls-1(a) congenic BALB.D2.Mls-1(a) mice were analyzed to examine directly the role of Mls-1(a) self-superantigens and V beta 6(+) T cells in autoimmune gastritis. Results: Autoimmune gastritis was detected in thymectomized BALB.D2.Mls-1(a) 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-1(a) mice. V beta 6(+) T cells were deleted in the stomach lymph nodes of 1-month-old gastritic BALB.D2.Mls-1(a) mice but could be detected by immunocytochemistry in the stomach lesions. Conclusions: Endogenous Mls-1(a) self-superantigens and Mls-1(a) reactive V beta 6(+) T cells are not involved in resistance to autoimmune gastritis in BALB.D2 mice.