Innate lymphoid cells prevent graft-versus-host disease via IL-9–driven T-cell senescence

D Dejene M. Tufa (Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO) E Eric Hoffmeyer (Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO) K Kristin L. Schaller (Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO) B Ben Kooiman (Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO) E Elena Woods (Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO) D Dong Wang D Dallas Jones (Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO) S Spencer Hall (Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO) J Joselyn Cruz Cruz (Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO) M Michael R. Verneris (Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO)

Abstract

Abstract Innate lymphoid cells (ILCs) are tissue-resident lymphocytes that regulate tissue homeostasis and immune responses. How ILCs modulate T cells, remains incompletely understood. To investigate the interaction between ILCs and T cells, we differentiated ILC2s and ILC3s from hematopoietic stem cells (HSCs). Both suppressed T-cell proliferation, enhanced cytokine production, and upregulated T-cell senescence–associated surface receptors (CD57, KLRG1, TIGIT, and TIM3). T cells exposed to ILCs also increased expression of senescence-related proteins, including p16, p21, p53, GATA4, and NF-κB. Mechanistically, ILCs produced interleukin-9 (IL-9), and IL-9 blockade prevented ILC-driven T-cell senescence. Conversely, addition of exogenous IL-9 to T cells recapitulated the effects of ILC coculture. Finally, in both human xenogeneic and murine allogeneic hematopoietic cell transplantation models, we observed ILC-mediated T-cell modulation in vivo, with evidence of T-cell senescence. In conclusion, HSC-derived ILCs from both humans and mice mitigate graft-versus-host disease by inducing T-cell senescence.

Article Details

Journal Blood
Volume / Issue Vol. 146, Issue 22
Published November 27, 2025
Pages 2656-2669
ISSN 0006-4971
Publisher Elsevier BV

Journal Info

Blood

Elsevier BV

ISSN: 0006-4971 Health Sciences

Authors (10)

D

Dejene M. Tufa

Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO

E

Eric Hoffmeyer

Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO

K

Kristin L. Schaller

Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO

B

Ben Kooiman

Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO

E

Elena Woods

Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO

D

Dong Wang

D

Dallas Jones

Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO

S

Spencer Hall

Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO

J

Joselyn Cruz Cruz

Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO

M

Michael R. Verneris

Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO