- 作者: Ping-Nig Hsu Hsin-Hui Lin Chin-Fu Tu Nien-Jung Chen Kang-Mai Wu Hwei-Fang Tsai Shie-Liang Hsieh
- 作者服務機構: Graduate Institute of Immunology, College of Medicine, National taiwan University, taipei, Pig research Institute Taiwan, Chunan, Department of Microbiology and Immunology, National Yang-Ming University, Shihpai, Taipei, Taiwan, ROC
- 中文摘要: --
- 英文摘要: Fas (CD95) and Fas ligand (FasL/CD95L) are involved inprogrammed cell death and the regulation of host im-mune responses. Fast has been shown to provide im-mune privilege, thus prolonging the survival of un-matched grafts in a variety of tissues, such as eyes andtestis. In murine FasL (mFasL) transgenic mice, FasL pro-voked granulocyte infiltration and insulitis in the pan-creas. We intended to study whether the expression ofhuman FasL, instead of mFasL, on mouse (β islet cellscould avoid granulocyte infiltration, and whether isletcells transgenic for FasL could be used in islet transplan-tation. We produced transgenic mice in which the humanFasL transgene was driven by rat insulin promoter andwas expressed exclusively in the pancreas islet cells inICR mice. In contrast to mFasL transgenic mice, histo-chemical staining showed thatthe pancreas was intact inhuman FasL transgenic ICR mice. However, when hu-man FasL transgenic islet cells were transplanted intoallogeneic mice with streptozotocin-induced diabetes,human Fast appeared not to prolong graft survival.Intensive granulocyte infiltration into the islet grafts wasobserved in recipients (Balb/c mice) which received isletgrafts from human FasL transgenic mice, but not fromnontransgenic, allogeneic ICR mice on day 31. Our ob-servations suggest that FasL alone is insufficient to con-fer immune protection, and that other environmental fac-tors might contribute to the formation of immune privi-lege sites in vivo
- 中文關鍵字: --
- 英文關鍵字: Human Fas Ligand. Islet cells. Murine allogeneic islet transplantation. Immune privilege