Journal of advanced research · 2026
CD52+ cells are associated with faster short-term neutrophil recovery in mobilized hematopoietic stem cell transplant.
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Chen Li, Wang Xiaojie, Wang Xiaoqi, Hu Lanyue, Tan Chengning, Yin Xiaoting, Zhang Genling, Miao Yingying, Wang Maolin, Xiang Lixin, Xiao Yanni, Yang Zhenxing, Xiang Yang, Chen Maoshan, Ran Qian, Li Zhongjun
Аннотация
INTRODUCTION: Delayed neutrophil recovery after peripheral blood hematopoietic stem cell transplantation (PBHSCT) remains a leading driver of post-transplant infections and is closely associated with adverse outcomes. Current graft potency assessments rely on bulk CD34+ cell counts, which fail to resolve functional heterogeneity within the CD34+ compartment and poorly predict short-term engraftment outcomes.
OBJECTIVES: We aimed to identify a CD34+ subpopulation that robustly predicts accelerated neutrophil recovery, define its biological basis, and evaluate its clinical utility for optimizing PBHSCT management.
METHODS: We profiled G-CSF-mobilized CD34+ grafts from 30 paired HLA-matched healthy donors and acute leukemia recipients across discovery (n = 9) and validation (n = 21) cohorts using single-cell RNA sequencing (scRNA-seq) and multicolor flow cytometry. Findings were validated via in vitro multi-lineage differentiation, single-cell cloning, xenotransplantation, and rigorous statistical approaches including bootstrap resampling and robust regression.
RESULTS: We identified Lin-CD34+ CD52+ cells as a myeloid-primed subpopulation whose dose correlated strongly with shortened interval to neutrophil recovery (INR) than bulk CD34+ or canonical HSPC subsets (R = -0.87, p < 0.001). High-dose recipients reached the clinical recovery threshold (0.5 × 109/L) 2 days earlier than low-dose counterparts. Mechanistically, Lin-CD34+ CD52+ cells exhibited hyperactivated SPI1/PU.1 signalling and a G-CSF-induced pro-migratory signature absent in steady-state bone marrow CD34+ cells. Crucially, CD52 blockade did not alter progenitor function, confirming CD52 as a passive surrogate marker of myeloid priming rather than an active differentiation driver.
CONCLUSION: Our findings establish CD52 as a novel, clinically actionable biomarker for PBHSCT graft potency, supporting potency-informed graft selection and individualized transplant planning to accelerate neutrophil recovery and improve patient outcomes.
OBJECTIVES: We aimed to identify a CD34+ subpopulation that robustly predicts accelerated neutrophil recovery, define its biological basis, and evaluate its clinical utility for optimizing PBHSCT management.
METHODS: We profiled G-CSF-mobilized CD34+ grafts from 30 paired HLA-matched healthy donors and acute leukemia recipients across discovery (n = 9) and validation (n = 21) cohorts using single-cell RNA sequencing (scRNA-seq) and multicolor flow cytometry. Findings were validated via in vitro multi-lineage differentiation, single-cell cloning, xenotransplantation, and rigorous statistical approaches including bootstrap resampling and robust regression.
RESULTS: We identified Lin-CD34+ CD52+ cells as a myeloid-primed subpopulation whose dose correlated strongly with shortened interval to neutrophil recovery (INR) than bulk CD34+ or canonical HSPC subsets (R = -0.87, p < 0.001). High-dose recipients reached the clinical recovery threshold (0.5 × 109/L) 2 days earlier than low-dose counterparts. Mechanistically, Lin-CD34+ CD52+ cells exhibited hyperactivated SPI1/PU.1 signalling and a G-CSF-induced pro-migratory signature absent in steady-state bone marrow CD34+ cells. Crucially, CD52 blockade did not alter progenitor function, confirming CD52 as a passive surrogate marker of myeloid priming rather than an active differentiation driver.
CONCLUSION: Our findings establish CD52 as a novel, clinically actionable biomarker for PBHSCT graft potency, supporting potency-informed graft selection and individualized transplant planning to accelerate neutrophil recovery and improve patient outcomes.