Eridani Sandro
Department of Biomedical Science and Technology, University of Milan, Milan, Italy.
Hematol Rep. 2011 Oct 19;3(3):e24. doi: 10.4081/hr.2011.e24. Epub 2011 Nov 4.
A linkage between presence of Sickle Haemoglobin (HbS) and protection from malaria infection and clinical manifestations in certain areas was suspected from early observations and progressively elucidated by more recent studies. Research has confirmed the abovementioned connection, but also clarified how such protection may be abolished by coexistence of sickle cell trait (HbS trait) and alpha thalassemia, which may explain the relatively low incidence of HbS trait in the Mediterranean. The mechanisms of such protective effect are now being investigated: factors of genetic, molecular and immunological nature are prominent. As for genetic factors attention is given to the role of the red blood cell (RBC) membrane complement regulatory proteins as polymorphisms of these components seem to be associated with resistance to severe malaria; genetic ligands like the Duffy group blood antigen, necessary for erythrocytic invasion, and human protein CD36, a major receptor for P. falciparum-infected RBC's, are also under scrutiny: attention is focused also on plasmodium erythrocyte-binding antigens, which bind to RBC surface components. Genome-wide linkage and association studies are now carried out too, in order to identify genes associated with malaria resistance. Only a minor role is attributed to intravascular sickling, phagocytosis and haemolysis, while specific molecular mechanisms are the object of intensive research: among these a decisive role is played by a biochemical sequence, involving activation of haeme oxygenase (HMO-1), whose effect appears mediated by carbon monoxide (CO). A central role in protection from malaria is also played by immunological factors, which may stimulate antibody production to plasmodium antigens in the early years of life; the role of agents like pathogenic CD8 T-cells has been suggested while the effects of molecular actions on the immunity mechanism are presently investigated. It thus appears that protection from malaria can be explained by interaction of different factors: the elucidation of such mechanisms may prove valuable for the prevention and treatment strategy of a disease which still affects large parts of the world.
早期观察就怀疑镰状血红蛋白(HbS)的存在与某些地区预防疟疾感染及临床表现之间存在联系,最近的研究则逐步阐明了这一联系。研究证实了上述关联,同时也阐明了镰状细胞性状(HbS性状)和α地中海贫血共存时如何消除这种保护作用,这或许可以解释地中海地区HbS性状发病率相对较低的原因。目前正在研究这种保护作用的机制:遗传、分子和免疫性质的因素较为突出。关于遗传因素,人们关注红细胞(RBC)膜补体调节蛋白的作用,因为这些成分的多态性似乎与对严重疟疾的抗性有关;对于红细胞入侵所必需的达菲血型抗原等遗传配体以及恶性疟原虫感染的红细胞的主要受体人类蛋白CD36也在进行研究:人们还将注意力集中在与红细胞表面成分结合的疟原虫红细胞结合抗原上。现在也在进行全基因组连锁和关联研究,以确定与疟疾抗性相关的基因。血管内镰变、吞噬作用和溶血作用仅起次要作用,而特定的分子机制则是深入研究的对象:其中一个由血红素加氧酶(HMO-1)激活介导的生化序列起决定性作用,其作用似乎由一氧化碳(CO)介导。免疫因素在预防疟疾中也起着核心作用,它可能在生命早期刺激针对疟原虫抗原的抗体产生;有人提出致病性CD8 T细胞等因子的作用,目前正在研究分子作用对免疫机制的影响。因此,似乎可以通过不同因素的相互作用来解释对疟疾的保护作用:阐明这些机制可能对这种仍在世界大部分地区流行的疾病的预防和治疗策略具有重要价值。