Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095-1652, USA.
Transplant Rev (Orlando). 2011 Oct;25(4):154-66. doi: 10.1016/j.trre.2011.04.001. Epub 2011 Jul 30.
Experimental evidence indicates that donor-specific antibodies targeting major histocompatibility complex classes I and II molecules can elicit the key features of transplant vasculopathy by acting on the graft vasculature in 3 ways: directly activating proliferative, prosurvival, and migratory signaling in the target endothelial and smooth muscle cells; increasing expression of mitogenic factors in vascular endothelial cells, creating a potential proliferative autocrine loop; and promoting recruitment of inflammatory cells that produce mitogenic factors and elicit chronic inflammation, proliferation, and fibrosis. Here, we review the experimental literature showing the complement and Fc-independent effects of major histocompatibility complex classes I and II antibodies on graft vascular cells that may directly contribute to the proliferative aspect of transplant vasculopathy.
实验证据表明，针对主要组织相容性复合物 I 类和 II 类分子的供体特异性抗体可以通过以下 3 种方式作用于移植物血管来引发移植血管病的关键特征：直接激活靶内皮细胞和平滑肌细胞中的增殖、生存和迁移信号；增加血管内皮细胞中有丝分裂原因子的表达，形成潜在的增殖自分泌环；促进产生有丝分裂原因子并引发慢性炎症、增殖和纤维化的炎症细胞募集。在这里，我们回顾了实验文献，显示了主要组织相容性复合物 I 类和 II 类抗体对移植物血管细胞的补体和 Fc 非依赖性作用，这些作用可能直接导致移植血管病的增殖方面。
