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ÀÌ¿µÃ¶ ( Lee Young-Cheol ) 
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±èÁ¤Áø ( Kim Jeong-Jin ) 
ÇѸ²´ëÇб³ ÀÇ°ú´ëÇÐ ¿Ü°úÇб³½Ç
¹ÚÇý¸² ( Park Hye-Rim ) 
ÇѸ²´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç
À̻■ ( Lee Sam-Uel ) 
ÇѸ²´ëÇб³ ÀÇ°ú´ëÇÐ ¿Ü°úÇб³½Ç
¿ì¿µ¹Î ( Woo Young-Min ) 
ÇѸ²´ëÇб³ ÀÇ°ú´ëÇÐ ÀϹݿܰúÇб³½Ç
Á¶¸¶ÇØ ( Cho Ma-Hae ) 
ÇѸ²´ëÇб³ ÀÇ°ú´ëÇÐ ¿Ü°úÇб³½Ç
±èÁÖ¼· ( Kim Joo-Seop ) 
ÇѸ²´ëÇб³ ÀÇ°ú´ëÇÐ ¿Ü°úÇб³½Ç
À̺ÀÈ­ ( Lee Bong-Wha ) 
ÇѸ²´ëÇб³ ÀÇ°ú´ëÇÐ ¿Ü°úÇб³½Ç

Abstract


Purpose: Mouse liver nonparenchymal cells play an important role n the development of active apoptosis in graftinfiltrating 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 eble 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¡¾13.2% at E/T ratio=12.5/1) compared with spleen cells as effectors (4.7¡¾13.4% 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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°£ ¼ö»ó¼¼Æ÷;T ÀÓÆı¸;Bax;Liver dendritic cells;T cell apoptosis

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