The effect of nitric oxide on allograft rejection

免疫能态细胞介导同种异体移植物损伤组织的机制仍存在争议。许多实验支持同种异体致敏细胞毒性T细胞（CTL）和非特异性炎症介质在移植物排斥反应中起关键作用的观点。我们通过直接体外细胞毒性试验和移植物浸润细胞的限制稀释分析证明，DST可以阻止海绵基质同种异体移植物中CTL活性的发展。在小鼠海绵异体移植模型中，DST还与通过增强PGE2产生抑制NO合成有关。他克莫司抑制CTL活性和NO的产生。然而，IFNgamma/LPS再刺激后，移植物浸润细胞的NO生成增加。NOS抑制剂抑制同种异体DTH。NO与体内、体外免疫调节作用均有显著相关。NO也可以作为免疫激活的标志。

The mechanisms by which immune competent cells mediate allograft injury tissue is still controversial. Many experiments support the view the allosensitized cytotoxic T cells (CTL) and non-specific inflammatory mediators play a crititcal role in graft rejection.We demonstrated that DST prevented the development of CTL activity in the sponge matrix allograft as demonstrated by both direct in vitro cytotoxicity assays and limiting dilution analysis of graft infiltrating cells. DST was also associated with depressed NO synthesis by enhanced PGE2 production in the murine sponge allograft model.Tacrolimus suppressed the CTL activity and NO production. However, NO production of graft infiltrating cells increased after restimulation with IFNgamma/LPS.Allogeneic DTH was suppressed by NOS inhibitor.NO was related with immunoregulatory effects both in vitro and in vivo significantly. NO may be also effective as a marker of immune activation.