Orosz C G, van Buskirk A, Sedmak D D, Kincade P, Miyake K, Pelletier R P
College of Medicine, Department of Surgery, Ohio State University, Columbus 43210.
Immunol Lett. 1992 Mar;32(1):7-12. doi: 10.1016/0165-2478(92)90191-p.
Murine heterotopic cardiac isografts (C57B1/6----C57B1/6) undergo transient, non-destructive inflammation that is characterized by the acquisition of microvascular endothelial reactivity with the antibody MECA 32. Cardiac allografts (C57B1/6----DBA/2) undergo destructive inflammation that is characterized by the acquisition of reactivity with the antibody M/K-2, in addition to MECA 32. M/K-2 recognizes the murine endothelial adhesion molecule, VCAM-1. Hence, there appear to be antigen-dependent and antigen-independent forms of graft inflammation. Treatment of cardiac allograft recipients with 200 micrograms/day M/K-2 antibody retarded graft loss by only a few days, and did not interfere significantly with leukocytic infiltration, as detected by limiting dilution analysis of graft-reactive CTL, despite the fact that large amounts of M/K-2 could be detected on graft microvascular endothelia and in the peripheral blood as rejection progressed. These data indicate that VCAM is apparently not essential for the leukocytic infiltration and subsequent rejection of cardiac allografts, and is not involved in leukocytic infiltration of murine cardiac isografts.
小鼠异位心脏同基因移植（C57B1/6→C57B1/6）会经历短暂的、非破坏性的炎症反应，其特征是微血管内皮细胞与抗体MECA 32发生反应。心脏异基因移植（C57B1/6→DBA/2）会经历破坏性炎症反应，除了与MECA 32发生反应外，还表现为与抗体M/K-2发生反应。M/K-2识别小鼠内皮细胞粘附分子VCAM-1。因此，似乎存在抗原依赖性和抗原非依赖性的移植物炎症形式。用每天200微克的M/K-2抗体治疗心脏异基因移植受者，只能使移植物丢失延迟几天，并且对白细胞浸润没有明显干扰，这通过对移植物反应性CTL的极限稀释分析检测到，尽管随着排斥反应的进展，在移植物微血管内皮和外周血中可以检测到大量的M/K-2。这些数据表明，VCAM显然对于心脏异基因移植的白细胞浸润和随后的排斥反应不是必需的，并且不参与小鼠心脏同基因移植的白细胞浸润。
