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A Study for Apoptosis and Its Mechanism of Allogeneic Activated T Lymphocytes Induced by Mouse Liver Immature Dendritic Cells
Article en Ko | WPRIM | ID: wpr-174406
Biblioteca responsable: WPRO
ABSTRACT
PURPOSE: Mouse liver nonparenchymal cells play an important role in the development of active apoptosis in graft- infiltrating cytotoxic T lymphocytes, and this apoptosis can be an explanation for liver graft acceptance. We intended to clarify whether immature mouse liver dendritic cells can induce apoptosis in allogeneic activated T cells and determine which mechanism is involved in this phenomenon. METHODS: A radiometric DNA fragmentation test ("JAM" assay) was used to determine whether mouse liver dendritic cells were able to induce activated T-cell apoptosis in vitro. In addition, immunohistochemical staining for Bax and Bcl-2 was examined to clarify whether Bax or Bcl-2 was involved in this apoptosis. RESULTS: Immature mouse liver dendritic cells were quite strong inducers of activated T cell apoptotic death in allogeneic mice in vitro (39.2+/-13.2% at E/T ratio=12.5/1) compared with spleen cells as effectors (4.7+/-13.4% at E/T ratio=12.5/1) (P<0.0001). By using immunohistochemical staining, we also showed that Bax might play some role in this phenonenon, but that Bcl-2 might not. CONCLUSION: Our data indicate that immature mouse liver dendritic cells might have a strong apoptotic activity toward activated T cells in allogeneic mice in vitro through a Bax-involved mechanism.
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Texto completo: 1 Índice: WPRIM Asunto principal: Bazo / Células Dendríticas / Linfocitos T / Linfocitos T Citotóxicos / Apoptosis / Trasplantes / Fragmentación del ADN / Hígado Límite: Animals Idioma: Ko Revista: Journal of the Korean Surgical Society Año: 2004 Tipo del documento: Article
Texto completo: 1 Índice: WPRIM Asunto principal: Bazo / Células Dendríticas / Linfocitos T / Linfocitos T Citotóxicos / Apoptosis / Trasplantes / Fragmentación del ADN / Hígado Límite: Animals Idioma: Ko Revista: Journal of the Korean Surgical Society Año: 2004 Tipo del documento: Article