遗传增强
严重联合免疫缺陷
生物
免疫学
转基因
祖细胞
免疫缺陷
普通伽马链
病毒学
细胞因子
癌症研究
基因
免疫系统
干细胞
白细胞介素10
遗传学
作者
Marina Cavazzana,Salima Hacein‐Bey,Geneviève de Saint Basile,Fabian Gross,Éric Yvon,Patrick Nusbaum,Françoise Selz,Christophe Hue,Stéphanie Certain,Jean‐Laurent Casanova,Philippe Bousso,Françoise Le Deist,Alain Fischer
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2000-04-28
卷期号:288 (5466): 669-672
被引量:2622
标识
DOI:10.1126/science.288.5466.669
摘要
Severe combined immunodeficiency–X1 (SCID-X1) is an X-linked inherited disorder characterized by an early block in T and natural killer (NK) lymphocyte differentiation. This block is caused by mutations of the gene encoding the γc cytokine receptor subunit of interleukin-2, -4, -7, -9, and -15 receptors, which participates in the delivery of growth, survival, and differentiation signals to early lymphoid progenitors. After preclinical studies, a gene therapy trial for SCID-X1 was initiated, based on the use of complementary DNA containing a defective γc Moloney retrovirus–derived vector and ex vivo infection of CD34 + cells. After a 10-month follow-up period, γc transgene–expressing T and NK cells were detected in two patients. T, B, and NK cell counts and function, including antigen-specific responses, were comparable to those of age-matched controls. Thus, gene therapy was able to provide full correction of disease phenotype and, hence, clinical benefit.
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