Temporal dynamics of TNF-mediated changes in hematopoietic stem cell function and recovery
(2023) In iScience 26(4).- Abstract
While tumor necrosis factor (TNF) is a critical mediator of appropriate immune response and tissue repair, its misregulation is linked to cancer, autoimmunity, bone marrow failure, and aging. Understanding the context-dependent roles of TNF is essential for elucidating normal and pathogenic conditions and to guide clinical therapy advancements. Prior studies suggested that TNF restricts the self-renewal capacity of hematopoietic stem cells (HSCs), but its long-term effect on HSCs remains unclear. Here, we demonstrate that in vivo TNF administration results in a transient exit of HSCs from quiescence, which coincides with a compromised repopulation capacity. These functional changes are; however, fully reversible even following... (More)
While tumor necrosis factor (TNF) is a critical mediator of appropriate immune response and tissue repair, its misregulation is linked to cancer, autoimmunity, bone marrow failure, and aging. Understanding the context-dependent roles of TNF is essential for elucidating normal and pathogenic conditions and to guide clinical therapy advancements. Prior studies suggested that TNF restricts the self-renewal capacity of hematopoietic stem cells (HSCs), but its long-term effect on HSCs remains unclear. Here, we demonstrate that in vivo TNF administration results in a transient exit of HSCs from quiescence, which coincides with a compromised repopulation capacity. These functional changes are; however, fully reversible even following prolonged/chronic transient exposure to TNF. Notably, antagonizing TNF signaling in transplantation recipients enhances donor HSC reconstitution. Our findings provide molecular and functional insight into HSC regulation, with implications for both acute and chronic inflammatory conditions.
(Less)
- author
- Rundberg Nilsson, Alexandra LU ; Hidalgo, Isabel LU ; Bryder, David LU and Pronk, Cornelis Jan
- organization
- publishing date
- 2023-04-21
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Biological sciences, Cell biology, Molecular biology, Stem cells research
- in
- iScience
- volume
- 26
- issue
- 4
- article number
- 106341
- publisher
- Elsevier
- external identifiers
-
- pmid:36968066
- scopus:85150262885
- ISSN
- 2589-0042
- DOI
- 10.1016/j.isci.2023.106341
- language
- English
- LU publication?
- yes
- id
- 0888aa20-b0c2-49db-8884-2e4a4d3a3e09
- date added to LUP
- 2023-04-24 12:18:29
- date last changed
- 2024-11-16 19:03:04
@article{0888aa20-b0c2-49db-8884-2e4a4d3a3e09, abstract = {{<p>While tumor necrosis factor (TNF) is a critical mediator of appropriate immune response and tissue repair, its misregulation is linked to cancer, autoimmunity, bone marrow failure, and aging. Understanding the context-dependent roles of TNF is essential for elucidating normal and pathogenic conditions and to guide clinical therapy advancements. Prior studies suggested that TNF restricts the self-renewal capacity of hematopoietic stem cells (HSCs), but its long-term effect on HSCs remains unclear. Here, we demonstrate that in vivo TNF administration results in a transient exit of HSCs from quiescence, which coincides with a compromised repopulation capacity. These functional changes are; however, fully reversible even following prolonged/chronic transient exposure to TNF. Notably, antagonizing TNF signaling in transplantation recipients enhances donor HSC reconstitution. Our findings provide molecular and functional insight into HSC regulation, with implications for both acute and chronic inflammatory conditions.</p>}}, author = {{Rundberg Nilsson, Alexandra and Hidalgo, Isabel and Bryder, David and Pronk, Cornelis Jan}}, issn = {{2589-0042}}, keywords = {{Biological sciences; Cell biology; Molecular biology; Stem cells research}}, language = {{eng}}, month = {{04}}, number = {{4}}, publisher = {{Elsevier}}, series = {{iScience}}, title = {{Temporal dynamics of TNF-mediated changes in hematopoietic stem cell function and recovery}}, url = {{http://dx.doi.org/10.1016/j.isci.2023.106341}}, doi = {{10.1016/j.isci.2023.106341}}, volume = {{26}}, year = {{2023}}, }