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血型抗原可将感染因子作为受体与疾病直接关联,或间接被宿主的免疫反应干扰。只有少数感染因子,如:疟原虫、细小病毒B19影响红细胞及其前体。大多数感染因子附着在红细胞上,把它们作为靶器官的载体,或附着在粘膜表达的血型抗原上。 血型抗原与疾病之间的一些关系可起因于它们与补体系统的关系:KN抗原(Kn,McC和Yk)位于补体Ⅰ型受体分子(C R1)上,CR1存在于RBCs、淋巴细胞、巨噬细胞、树突状细胞及单核细胞上。RBCs上的CR1数量在免疫学疾病发生时减少,如获得性免疫缺乏症、系统性红斑狼疮及一些肿瘤。 获得性和先天性遗传疾病 正常RBC表面含有糖基磷脂酰肌醇GPI联结蛋白,GPI调节因子在阵发性睡眠性血红蛋白尿个体中缺失,使RBC对补体介导的溶解更敏感,受影响的RBC缺失所有Cromer、Yt、JMH、Do和Emm血型抗原。
Blood group antigens can directly affect the infectious agent as a receptor and disease or indirectly interfere with the host’s immune response. Only a few infectious agents, such as Plasmodium, and Parvovirus B19 affect erythrocytes and their precursors. Most infectious agents attach to red blood cells, use them as a target organ carrier, or adhere to mucosal-expressed blood group antigens. Some of the relationships between blood group antigens and diseases may arise from their relationship to the complement system: the KN antigens (Kn, McC and Yk) are located on the complement type I receptor molecule (CRI) and CR1 is present on RBCs, lymphocytes, Phagocytes, dendritic cells and monocytes. The number of CR1 on RBCs is reduced when immunological diseases occur, such as acquired immune deficiency syndrome, systemic lupus erythematosus and some tumors. Acquired and Congenital Genetic Disorders Normal RBCs contain glycosylphosphatidylinositol GPI-linked protein, GPI regulators missing in patients with paroxysmal nocturnal hemoglobinuria, making RBC more sensitive to complement-mediated lysis RBC is depleted of all Cromer, Yt, JMH, Do and Emm blood group antigens.