Kennedy James Randall
All Children's Hospital, St. Petersburg, USA.
Med Sci Monit. 2002 May;8(5):HY10-3.
This paper's focus is prevention of sickle cell adhesion resulting from the erythrocyte's prematurely denatured hemoglobin. This denatured hemoglobin causes a molecule called band 3 to cluster on the erythrocyte's surface and adhere to the CD36 molecule located on the microvascular endothelium. Natural antibodies recognize these clusters on senescent erythrocytes and prevent their endothelial adhesion and target them for reticuloendothelial elimination. Band 3 is also displayed on the erythrocytes of individuals with falciparum malaria and the vaso-occlusive pathology in these patients is prevented in individuals with sickle trait. The hypothesis is that prematurely denatured sickle hemoglobin results in an up regulation of natural antibodies which control erythrocyte adhesion in both malaria and sickle cell disease.
本文的重点是预防由红细胞中过早变性的血红蛋白导致的镰状细胞黏附。这种变性的血红蛋白会使一种名为带3的分子聚集在红细胞表面,并与位于微血管内皮上的CD36分子黏附。天然抗体识别衰老红细胞上的这些聚集物,防止它们与内皮细胞黏附,并将其作为目标进行网状内皮清除。带3也会出现在恶性疟患者的红细胞上,而镰状细胞性状个体可预防这些患者的血管阻塞性病变。假说认为,过早变性的镰状血红蛋白会导致天然抗体上调,从而在疟疾和镰状细胞病中控制红细胞黏附。