@misc{oai:niigata-u.repo.nii.ac.jp:00004881,
 author = {Fujii, Masato},
 month = {Mar},
 note = {Neonatal thymectomy induces autoimmune gastritis in relatively higher incidence in BALB/c mice, whereas DBA/2 mice are quite resistant. The incidence of AIG has been thought to be related with activation of Vβ6^+ T cells reacting Minor lymphocyte stimulating (Mls)-la antigens because the susceptible BALB/c mouse is Mls-la-negative, while DBA/2 mouse is Mls-la-positive. Supporting this idea, a proportion of Vβ6^+, but not of Vβ8^+, T cells increased in AIG NTx BALB/c mice and these mice were up-regulated in IFN-γ production from young. Conversely, the deletion of Vβ6^+ T cells in BALB/c mice by transplantation of DBA/2 bone marrow cells as neonate resulted in decreasing the incidence of AIG. However, it was surprising that these chimeric mice lacking Vβ6^+ T cells possessed autoreactive T cells which could transfer the disease in nude mice. Moreover, Vβ6^+ T cells which deleted by transplantation of bone marrow cells from Mls-la^+ mice possessing BALB/c genetic background could not make BALB/c mice resistant. Thus, the presence or absence of Mls-la antigens would not be involved in the initiation of AIG. On the other hand, IFN-γ-producing CD4^+ T cells of NTx BALB/c mice were decreased by transplanted with DBA/2 bone marrow cells as neonate: NTx DBA/2-chimeric BALB/c mice were thought to be under the anti-inflammatory state. Indeed, DBA/2-originated myeloid cells showed increased IL-10-production. These results indicate that the controlling mechanism for the AIG incidence is on the secreted quantity of anti-inflammatory cytokine from myeloid cells under the genetic control. A unique pathological feature of murine autoimmune gastritis (AIG) in mice is its pronounced mucosal hypertrophy, which is different from human type-A chronic atrophic gastritis with pernicious anemia. The aim of this study was to clarify the mechanism of gastric hypertrophy in murine AIG, especially in relation to inflammatory cells infiltrating in the gastric mucosa. Neonatally thymectomized (NTx) BALB/c and (BALB/c×DBA/2) F1 mice with gastritis were examined histologically and serologically. The T-helper (Th1/Th2) immune balance in the spleen was evaluated by intracellular cytokine staining for interferon-γ and flow-cytometric beads array for several cytokines. Additionally, AIG NTx BALB/c mice were orally administered with an H_2-blocker to decrease eosinophils. Obtained results are as follows: AIG NTx BALB/c mice exhibited gastritis without stomach hypertrophy at two months old, and developed gastritis with mucous gland hypertrophy accompanied with eosinophil infiltration at six months old. In contrast, AIG NTx (BALB/c×DBA/2) F1 mice displayed gastritis with neither stomach hypertrophy nor eosinophil infiltration even at the age of six months. Upregulation of IL-4 and GM-CSF in the spleen was observed in BALB/c mice but not in (BALB/c×DBA/2) F1 mice. Additionally, some AIG NTx BALB/c mice did not show gastric hypertrophy or eosinophil infiltration due to the administration of an H_2-blocker. As conclusions, there are two different pathological phenotypes of murine autoimmune gastritis: chronic gastritis and hypertrophic gastritis in AIG NTx BALB/c mice. Furthermore, eosinophil infiltration and Th2 immune response might play a key role in the phenotypic shift from chronic gastritis into hypertrophic gastritis in AIG NTx BALB/c mice., 新大院博（理）甲第276号},
 title = {Thymus and self-unresponsiveness : Cellular and molecular basis for the generation of autoimmunity in neonatally thymectomized mice},
 year = {2007}
}