CD28+ CD8+ Tem cells with a STAT1-dependent glucocorticoid receptor deficit contribute to steroid-refractory acute GVHD

Z Zengkai Pan (1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China) Y Yujun Deng (Stanford Institute for Materials and Energy Sciences) J Jingtao Huang H Haoxing Bian (1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China) Y Yiyin Chen A Aijie Huang C Chuanhe Jiang (1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China) L Luxiang Wang (State Key Laboratory of Chemistry and Utilization of Carbon Based Energy Resources College of Chemistry Xinjiang University Urumqi China) Z Zilu Zhang (State Key Laboratory of Elemento-Organic Chemistry, State Key Laboratory of Advanced Chemical Power Sources, College of Chemistry) H Haiyang Lü S Su Li (State Key Laboratory of Coal Conversion, Institute of Coal Chemistry) T Tong Yin (Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Centre for Translational Medicine at Shanghai, Research Unit of Hematologic Malignancies Genomics and Translational Research of Chinese Academy of Medical Sciences, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine) S Shanhe Yu (1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China) J Jiang Zhu W Wei-Li Zhao (1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China) J Jianmin Wang (Key Laboratory of Advanced Energy Materials Chemistry (Ministry of Education), State Key Laboratory of Advanced Chemical Power Sources, College of Chemistry) J Jie Ji (State Key Laboratory of Inorganic Synthesis and Preparative Chemistry) Y Yang Xu H Hui Cheng J Jiahao Chen (Spin-X Institute, School of Chemistry and Chemical Engineering, School of Biomedical Sciences and Engineering, Guangdong-Hong Kong-Macao Joint Laboratory of Optoelectronic and Magnetic Functional Materials, State Key Laboratory of Luminescent Materials and Devices) H Hongbo Hu X Xiaoxia Hu (1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China)

Abstract

Abstract Steroid-refractory (SR) disease develops in a substantial fraction of patients with grade II to IV acute graft-versus-host disease (aGVHD) and is associated with poor long-term survival. Improved mechanistic insight is needed to identify reliable predictors of steroid resistance. We retrospectively profiled peripheral blood collected before glucocorticoid treatment from allogeneic hematopoietic cell transplantation recipients without aGVHD, with steroid-sensitive aGVHD, and with SR-aGVHD using an integrated multiomics approach, and validated our findings in an independent multicenter cohort. Mass cytometry revealed an expansion of activated CD28+ CD8+ effector-memory T (Tem) cells in SR-aGVHD. Absolute counts of these cells at neutrophil engraftment predicted subsequent steroid resistance in the multicenter cohort and performed comparably to established clinical classifiers. This phenotype was associated with a proinflammatory milieu enriched in interleukin-2 (IL-2), IL-27, and interferon gamma. Single-cell RNA sequencing and functional assays implicated a STAT1–glucocorticoid receptor (GR) regulatory axis, in which inflammatory cytokines induce STAT1 phosphorylation and suppress GR expression, consistent with intrinsic glucocorticoid resistance. JAK inhibition rescued cytokine-induced steroid resistance in vitro, whereas in patients with SR-aGVHD, clinical response to ruxolitinib was accompanied by reduced STAT1 activation, restoration of GR expression, and contraction of the expanded CD8+ Tem cell pool. These findings identify immune dysregulation in SR-aGVHD centered on CD8+ Tem cells with a STAT1-dependent GR deficit and support a mechanistic link to steroid refractoriness. CD28+ CD8+ Tem cell counts may serve as a biomarker of SR-aGVHD and inform the development of preemptive, pathway-targeted therapeutic strategies.

Article Details

Journal Blood
Volume / Issue Vol. 148, Issue 1
Published July 02, 2026
Pages 130-144
ISSN 0006-4971
Publisher Elsevier BV

Journal Info

Blood

Elsevier BV

ISSN: 0006-4971 Health Sciences

Authors (22)

Z

Zengkai Pan

1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

Y

Yujun Deng

Stanford Institute for Materials and Energy Sciences

J

Jingtao Huang

H

Haoxing Bian

1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

Y

Yiyin Chen

A

Aijie Huang

C

Chuanhe Jiang

1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

L

Luxiang Wang

State Key Laboratory of Chemistry and Utilization of Carbon Based Energy Resources College of Chemistry Xinjiang University Urumqi China

Z

Zilu Zhang

State Key Laboratory of Elemento-Organic Chemistry, State Key Laboratory of Advanced Chemical Power Sources, College of Chemistry

H

Haiyang Lü

S

Su Li

State Key Laboratory of Coal Conversion, Institute of Coal Chemistry

T

Tong Yin

Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Centre for Translational Medicine at Shanghai, Research Unit of Hematologic Malignancies Genomics and Translational Research of Chinese Academy of Medical Sciences, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine

S

Shanhe Yu

1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

J

Jiang Zhu

W

Wei-Li Zhao

1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

J

Jianmin Wang

Key Laboratory of Advanced Energy Materials Chemistry (Ministry of Education), State Key Laboratory of Advanced Chemical Power Sources, College of Chemistry

J

Jie Ji

State Key Laboratory of Inorganic Synthesis and Preparative Chemistry

Y

Yang Xu

H

Hui Cheng

J

Jiahao Chen

Spin-X Institute, School of Chemistry and Chemical Engineering, School of Biomedical Sciences and Engineering, Guangdong-Hong Kong-Macao Joint Laboratory of Optoelectronic and Magnetic Functional Materials, State Key Laboratory of Luminescent Materials and Devices

H

Hongbo Hu

X

Xiaoxia Hu

1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China