Immunobiology of rejection and adaptation
Immunobiology of rejection and adaptation
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DOI：
10.1016/j.transproceed.2007.01.047
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发表时间：
2007-04-01
影响因子：
0.9
通讯作者：
Trivedi, H. L.
中科院分区：
文献类型：
--
作者：
Trivedi, H. L.
移植是器官衰竭的一种可接受的治疗方法，然而，预防急性排斥反应和免疫抑制剂诱导的毒性之间的平衡仍然难以捉摸。来自基因完全不同的供体的器官移植诱导了受体对供体抗原的免疫反应。这些反应的不受控制的累积效应可能危及受体的生命并破坏移植组织。来自同种异体移植物的旅客白细胞形式的供体抗原迁移到有组织的淋巴细胞集合是急性排斥反应开始的先决条件。在宿主淋巴组织中，供体特异性树突状细胞通过供体肽激活初始CD4辅助T细胞，进而通过释放细胞因子激活效应CD8 T细胞克隆。活化的效应CD8细胞返回移植物，并在粘附分子和穿孔素的帮助下增强破坏活性。这似乎是适应性免疫破坏病毒病原体的机制；同种异体移植物的损伤模式没有太大的不同。适应性和耐受性是基于供体特异性免疫反应通过激活-删除-衰竭途径耗尽的原则。
Transplantation is an acceptable therapy for failing organs, however, the balance between prevention of acute rejection and immunosuppressant-induced toxicity remains elusive. Organ transplantation from a genetically disparate donor induces an immune response toward donor antigens in the recipient. An uncontrolled cumulative effect of these responses may jeopardize the recipient's life and destroy the grafted tissue. The donor antigen in the form of passenger leukocytes from the allograft migrating to the organized lymphoid collection is a prerequisite for initiation of acute rejection. In the host lymphoid tissue donor-specific dendritic cells primed with donor peptide activate naive CD4 helper T cells which in turn activate effector CD8 T-cell clones through the release of cytokines. Activated effector CD8 cells return to the graft and augment destructive activity with the help of adhesive molecules and perforin. This seems to be the mechanism of adaptive immunity to destroy viral pathogens; the pattern of allograft injury is not much different. Adaptation and tolerance are based on the principle of exhaustion of donor-specific immune responses by an activation-deletion-exhaustion pathway.