Matthews R J, Anson D S, Peake I R, Bloom A L
J Clin Invest. 1987 Mar;79(3):746-53. doi: 10.1172/JCI112880.
DNA from nine hemophilia B patients who produce anti-factor IX inhibitors (antibodies), including two brothers, was analyzed by the Southern blotting method and hybridization with factor IX cDNA, intragenomic, and 3'-flanking probes. Two inhibitor patients were shown to have total deletions of the factor IX gene. Two other inhibitor patients, the brothers, were shown to have a presumably identical complex rearrangement of the factor IX gene involving two separate deletions. The first deletion is of approximately 5.0 kb and removes exon e. The second deletion is between 9 and 29 kb and removes exons g and h but leaves exon f intact. An abnormal Taq I fragment at one end of the deletion junctions acted as a marker for the inheritance of hemophilia B in the patients' family. Five other inhibitor patients have a structurally intact factor IX gene as detected by this method. Our studies indicate that whereas large structural factor IX gene defects predispose hemophilia B patients to developing an anti-factor IX inhibitor, the development of an inhibitor can be associated with other defects of the factor IX gene.
采用Southern印迹法并使用因子IX cDNA、基因组内和3'侧翼探针,对包括两名兄弟在内的9名产生抗因子IX抑制剂(抗体)的B型血友病患者的DNA进行了分析。两名抑制剂患者显示因子IX基因完全缺失。另外两名抑制剂患者,即兄弟俩,显示因子IX基因发生了可能相同的复杂重排,涉及两个单独的缺失。第一次缺失约5.0 kb,缺失外显子e。第二次缺失在9至29 kb之间,缺失外显子g和h,但外显子f完整无损。缺失连接点一端的异常Taq I片段作为该患者家族中B型血友病遗传的标记。通过该方法检测,其他五名抑制剂患者的因子IX基因结构完整。我们的研究表明,虽然因子IX基因的大结构缺陷使B型血友病患者易产生抗因子IX抑制剂,但抑制剂的产生可能与因子IX基因的其他缺陷有关。