2018年9月19日，华东地区第15届实验动物科学学术交流会上，来自南昌大学生命科学研究院刘智志老师做了题为“chd7斑马鱼突变体与先天性免疫缺陷模型”的学术报告。

报告会上，刘老师提出了本项研究结论：Haematopoietic stem and progenitor cells, lymphoid progenitor cells, macrophages and neutrophils were increased but T cells was largely decreased upon chd7 knockdown or chd7 knockout；Organogenesis and homing function of the thymus were seriously impaired. Chd7 might regulate thymus organogenesis through modulating the development of both neural crest cell-derived mesenchyme and pharyngeal endoderm-derived thymic epithelial cells；The expression of foxn1, a central regulator of thymic epithelium, was remarkably downregulated in the pharyngeal region in chd7-deficient embryos；T-cell reduction in chd7-deficient embryos was partially rescued by overexpressing foxn1, suggesting that restoring thymic epithelium could be a potential therapeutic strategy for treating immunodeficiency in CHARGE syndrome.