比利时列日大学Christophe J. Desmet研究小组发现，单细胞蛋白质组学和转录组学捕捉嗜酸性粒细胞的发育过程，并确定IL-5在其谱系过渡放大中的作用。相关论文于2024年5月21日在线发表在《免疫》杂志上。

研究人员结合单细胞蛋白质组学和转录组学，生成了转基因IL-5Rα报告小鼠，以重新研究嗜酸性粒细胞的生成。研究人员协调了人类和小鼠的嗜酸性粒细胞生成，并在嗜酸性粒细胞成熟的不同阶段提供了广泛的细胞表面免疫表型和转录组。研究人员利用这些资源表明，IL-5通过转运扩增促进了嗜酸性粒细胞谱系的过渡放大，而其缺失或中和不会影响嗜酸性粒细胞的成熟。

根据该资源，研究人员还发现干扰素反应因子-8（被认为是骨髓造血的重要启动子）并非嗜酸性粒细胞造血所需。因此，这项工作为了解嗜酸性粒细胞的个体发育、当前精准疗法的效果以及健康和疾病中嗜酸性粒细胞发育和数量的调控提供了资源、方法和见解。

据了解，与其他免疫细胞相比，尽管使用了针对嗜酸性粒细胞生成促进细胞因子IL-5或其受体IL-5Rα的生物疗法，但嗜酸性粒细胞的活性、个体发生和谱系扩增机制仍未得到很好的研究。

附：英文原文

Title: Single-cell proteomics and transcriptomics capture eosinophil development and identify the role of IL-5 in their lineage transit amplification

Author: Joseph Jorssen, Glenn Van Hulst, Kiréna Mollers, Julien Pujol, Georgios Petrellis, Antonio P. Baptista, Sjoerd Schetters, Frédéric Baron, Jo Caers, Bart N. Lambrecht, Benjamin G. Dewals, Fabrice Bureau, Christophe J. Desmet

Issue&Volume: 2024-05-21

Abstract: The activities, ontogeny, and mechanisms of lineage expansion of eosinophils are lesswell resolved than those of other immune cells, despite the use of biological therapiestargeting the eosinophilia-promoting cytokine interleukin (IL)-5 or its receptor,IL-5Rα. We combined single-cell proteomics and transcriptomics and generated transgenicIL-5Rα reporter mice to revisit eosinophilopoiesis. We reconciled human and murineeosinophilopoiesis and provided extensive cell-surface immunophenotyping and transcriptomesat different stages along the continuum of eosinophil maturation. We used these resourcesto show that IL-5 promoted eosinophil-lineage expansion via transit amplification,while its deletion or neutralization did not compromise eosinophil maturation. Informedfrom our resources, we also showed that interferon response factor-8, considered anessential promoter of myelopoiesis, was not intrinsically required for eosinophilopoiesis.This work hence provides resources, methods, and insights for understanding eosinophilontogeny, the effects of current precision therapeutics, and the regulation of eosinophildevelopment and numbers in health and disease.

DOI: 10.1016/j.immuni.2024.04.027

Source: https://www.cell.com/immunity/abstract/S1074-7613(24)00232-2