A non-genotoxic stem cell therapy boosts lymphopoiesis and averts age-related blood diseases in mice
(2025) In Nature Communications 16(1).- Abstract
Hematopoietic stem cell (HSC) transplantation offers a cure for a variety of blood disorders, predominantly affecting the elderly; however, its application, especially in this demographic, is limited by treatment toxicity. In response, we employ a murine transplantation model based on low-intensity conditioning protocols using antibody-mediated HSC depletion. While aging presents a significant barrier to effective HSC engraftment, optimizing HSC doses and non-genotoxic targeting methods greatly enhance the long-term multilineage activity of the transplanted cells. We demonstrate that young HSCs, once effectively engrafted in aged hosts, improve hematopoietic output and ameliorate age-compromised lymphopoiesis. This culminated in a... (More)
Hematopoietic stem cell (HSC) transplantation offers a cure for a variety of blood disorders, predominantly affecting the elderly; however, its application, especially in this demographic, is limited by treatment toxicity. In response, we employ a murine transplantation model based on low-intensity conditioning protocols using antibody-mediated HSC depletion. While aging presents a significant barrier to effective HSC engraftment, optimizing HSC doses and non-genotoxic targeting methods greatly enhance the long-term multilineage activity of the transplanted cells. We demonstrate that young HSCs, once effectively engrafted in aged hosts, improve hematopoietic output and ameliorate age-compromised lymphopoiesis. This culminated in a strategy that robustly mitigates disease progression in a genetic model of myelodysplastic syndrome. These results suggest that non-genotoxic HSC transplantation could fundamentally change the clinical management of age-associated hematological disorders, offering a prophylactic tool to delay or even prevent their onset in elderly patients.
(Less)
- author
- Konturek-Ciesla, Anna
LU
; Zhang, Qinyu
LU
; Kharazi, Shabnam LU and Bryder, David LU
- organization
- publishing date
- 2025-12
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Nature Communications
- volume
- 16
- issue
- 1
- article number
- 5129
- publisher
- Nature Publishing Group
- external identifiers
-
- pmid:40456713
- scopus:105007095556
- ISSN
- 2041-1723
- DOI
- 10.1038/s41467-025-60464-3
- language
- English
- LU publication?
- yes
- id
- 948de61c-ffce-44c0-91d0-c95550c09f0f
- date added to LUP
- 2025-07-14 09:49:49
- date last changed
- 2025-07-15 03:28:21
@article{948de61c-ffce-44c0-91d0-c95550c09f0f, abstract = {{<p>Hematopoietic stem cell (HSC) transplantation offers a cure for a variety of blood disorders, predominantly affecting the elderly; however, its application, especially in this demographic, is limited by treatment toxicity. In response, we employ a murine transplantation model based on low-intensity conditioning protocols using antibody-mediated HSC depletion. While aging presents a significant barrier to effective HSC engraftment, optimizing HSC doses and non-genotoxic targeting methods greatly enhance the long-term multilineage activity of the transplanted cells. We demonstrate that young HSCs, once effectively engrafted in aged hosts, improve hematopoietic output and ameliorate age-compromised lymphopoiesis. This culminated in a strategy that robustly mitigates disease progression in a genetic model of myelodysplastic syndrome. These results suggest that non-genotoxic HSC transplantation could fundamentally change the clinical management of age-associated hematological disorders, offering a prophylactic tool to delay or even prevent their onset in elderly patients.</p>}}, author = {{Konturek-Ciesla, Anna and Zhang, Qinyu and Kharazi, Shabnam and Bryder, David}}, issn = {{2041-1723}}, language = {{eng}}, number = {{1}}, publisher = {{Nature Publishing Group}}, series = {{Nature Communications}}, title = {{A non-genotoxic stem cell therapy boosts lymphopoiesis and averts age-related blood diseases in mice}}, url = {{http://dx.doi.org/10.1038/s41467-025-60464-3}}, doi = {{10.1038/s41467-025-60464-3}}, volume = {{16}}, year = {{2025}}, }