Classically considered short-lived and purely defensive leukocytes, neutrophils are unique in their fast and moldable response to stimulation. This plastic behavior may underlie variable and even antagonistic functions during inflammation or cancer, yet the full spectrum of neutrophil properties as they enter healthy tissues remains unexplored. Using a new model to track neutrophil fates, we found short but variable lifetimes across multiple tissues. Through analysis of the receptor, transcriptional, and chromatin accessibility landscapes, we identify varying neutrophil states and assign non-canonical functions, including vascular repair and hematopoietic homeostasis. Accordingly, depletion of neutrophils compromised angiogenesis during early age, genotoxic injury, and viral infection, and impaired hematopoietic recovery after irradiation. Neutrophils acquired these properties in target tissues, a process that, in the lungs, occurred in CXCL12-rich areas and relied on CXCR4. Our results reveal that tissues co-opt neutrophils en route for elimination to induce programs that support their physiological demands.

传统上被认为是短命和纯粹防御性白细胞的嗜中性粒细胞在对刺激的快速和可塑性反应方面是独一无二的。这种可塑性行为可能是炎症或癌症期间可变甚至拮抗功能的基础，但中性粒细胞进入健康组织时的全部特性仍未得到探索。我们使用一种新模型来追踪嗜中性粒细胞的命运，发现其在多个组织中的寿命很短但变化很大。通过对受体、转录和染色质可及性景观的分析，我们确定了不同的中性粒细胞状态并分配了非规范功能，包括血管修复和造血稳态。因此，中性粒细胞的耗竭会影响早期的血管生成、遗传毒性损伤和病毒感染，并会影响照射后的造血恢复。中性粒细胞在靶组织中获得了这些特性，这一过程在肺部发生在富含 CXCL12 的区域并依赖于 CXCR4。我们的结果表明组织选择了中性粒细胞在消除过程中诱导支持其生理需求的程序。