Dufter C, Watzlik A, Opelz G, Terness P
Department of Transplantation Immunology, University of Heidelberg, Germany.
Transpl Int. 1998;11 Suppl 1:S361-3. doi: 10.1007/s001470050498.
We have defined factors relevant for the induction of rejection by indirect recognition in a rat heart allograft model and analyzed the influence of CTLA4Ig treatment on indirect alloactivation induced by donor MHC I peptides in a DA-->LEW heart allograft model. Indirect allorecognition of MHC I led to accelerated graft rejection and was accompanied by the induction of anti-peptide antibodies and donor peptide-activated T cells. In an attempt to block the B7-induced costimulatory signal of T cell activation, CTLA4Ig was administered to graft recipients in addition to MHC I peptide treatment. CTLA4Ig therapy, however, was not effective in preventing the humoral or cellular anti-donor immune response, nor did it prevent accelerated graft rejection.
我们已经在大鼠心脏同种异体移植模型中定义了与间接识别诱导排斥反应相关的因素，并分析了CTLA4Ig治疗对DA→LEW心脏同种异体移植模型中供体MHC I肽诱导的间接同种异体激活的影响。对MHC I的间接同种异体识别导致移植排斥加速，并伴有抗肽抗体的诱导和供体肽激活的T细胞。为了阻断B7诱导的T细胞激活共刺激信号，除了给予MHC I肽治疗外，还对移植受体给予CTLA4Ig。然而，CTLA4Ig治疗在预防体液或细胞抗供体免疫反应方面无效，也不能预防移植排斥加速。
