Immunology Service, Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD.
Laboratory for Transcriptional Regulation, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan.
J Exp Med. 2021 Dec 6;218(12). doi: 10.1084/jem.20211118. Epub 2021 Oct 25.
AIOLOS/IKZF3 is a member of the IKAROS family of transcription factors. IKAROS/IKZF1 mutations have been previously associated with different forms of primary immunodeficiency. Here we describe a novel combined immunodeficiency due to an IKZF3 mutation in a family presenting with T and B cell involvement, Pneumocystis jirovecii pneumonia, and/or chronic lymphocytic leukemia. Patients carrying the AIOLOS p.N160S heterozygous variant displayed impaired humoral responses, abnormal B cell development (high percentage of CD21low B cells and negative CD23 expression), and abrogated CD40 responses. Naive T cells were increased, T cell differentiation was abnormal, and CD40L expression was dysregulated. In vitro studies demonstrated that the mutant protein failed DNA binding and pericentromeric targeting. The mutant was fully penetrant and had a dominant-negative effect over WT AIOLOS but not WT IKAROS. The human immunophenotype was recapitulated in a murine model carrying the corresponding human mutation. As demonstrated here, AIOLOS plays a key role in T and B cell development in humans, and the particular gene variant described is strongly associated with immunodeficiency and likely malignancy.
AIOLOS/IKZF3 是 IKAROS 转录因子家族的成员。IKAROS/IKZF1 突变先前与不同形式的原发性免疫缺陷有关。在这里,我们描述了一个新的联合免疫缺陷,由一个家族中的 IKZF3 突变引起,该家族表现为 T 和 B 细胞受累、卡氏肺孢子虫肺炎和/或慢性淋巴细胞白血病。携带 AIOLOS p.N160S 杂合变体的患者表现出体液免疫反应受损、B 细胞发育异常(CD21low B 细胞比例高和 CD23 表达阴性)以及 CD40 反应缺失。幼稚 T 细胞增加,T 细胞分化异常,CD40L 表达失调。体外研究表明,突变蛋白无法进行 DNA 结合和着丝粒靶向。该突变具有完全外显率和显性负效应,可影响 WT AIOLOS,但不影响 WT IKAROS。在携带相应人类突变的小鼠模型中重现了人类免疫表型。正如本文所证明的,AIOLOS 在人类 T 和 B 细胞发育中起着关键作用,所描述的特定基因突变与免疫缺陷和可能的恶性肿瘤密切相关。