- Author
- Peter Tougaard (UGent) , Mario Ruiz Pérez (UGent) , Wolf Steels (UGent) , Jelle Huysentruyt, Bruno Verstraeten (UGent) , Jessica Vetters (UGent) , Tatyana Divert (UGent) , Amanda Gonçalves (UGent) , Ria Roelandt (UGent) , Nozomi Takahashi (UGent) , Sophie Janssens (UGent) , Terkild B. Buus, Tom Taghon (UGent) , Georges Leclercq (UGent) and Peter Vandenabeele (UGent)
- Organization
- Project
-
- Thymic reprogramming: The role of Death Receptor 3 (DR3)
- Factors that determine RIPK1-dependent necroptosis
- Investigating the role of ferroptosis in acute liver injury and multiple sclerosis with newly developed chemical tool compounds
- Mechanisms of ferroptosis mediated immunoregulation
- MOlecular mechanisms of cellular DEath and Life decisions in Inflammation, Degeneration and Infection
- Cell Death Regulation and Role in Infection and Inflammatory Diseases
- Cell death activity regulation in inflammation and cancer
- Autophagy in inflammation and inflammatory disorders (ATLANTIS), from basic insights to experimental therapy
- Cell death modality regulation during immunotherapy (CREDIT): molecular mechanisms and experimental therapy.
- Improving cancer therapy by modulating cell death and the microbiome in the gut
- Abstract
- Acute thymic atrophy occurs following type 1 inflammatory conditions such as viral infection and sepsis, resulting in cell death and disruption of T cell development. However, the impact type 1 immunity has on thymic-resident innate lymphoid cells (ILCs) remains unclear. Single-cell RNA sequencing revealed neonatal thymic-resident type 1 ILCs (ILC1s) as a unique and immature subset compared to ILC1s in other primary lymphoid organs. Culturing murine neonatal thymic lobes with the type 1 cytokines interleukin-12 (IL-12) and IL-18 resulted in a rapid expansion and thymic egress of KLRG1(+)CXCR6(+) cytotoxic ILC1s. Live imaging showed the subcapsular thymic localization and exit of ILC1s following IL-12 + IL-18 stimulation. Similarly, murine cytomegalovirus infection in neonates resulted in thymic atrophy and subcapsular localization of thymic-resident ILC1s. Neonatal thymic grafting revealed that type 1 inflammation enhances the homing of cytokine-producing thymus-derived ILC1s to the liver and peritoneal cavity. Together, we show that type 1 immunity promotes the expansion and peripheral homing of thymic-derived ILC1s.
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-01HQWRBM7KWCVV58GW9MAMHRNB
- MLA
- Tougaard, Peter, et al. “Type 1 Immunity Enables Neonatal Thymic ILC1 Production.” SCIENCE ADVANCES, vol. 10, no. 3, 2024, doi:10.1126/sciadv.adh5520.
- APA
- Tougaard, P., Ruiz Pérez, M., Steels, W., Huysentruyt, J., Verstraeten, B., Vetters, J., … Vandenabeele, P. (2024). Type 1 immunity enables neonatal thymic ILC1 production. SCIENCE ADVANCES, 10(3). https://doi.org/10.1126/sciadv.adh5520
- Chicago author-date
- Tougaard, Peter, Mario Ruiz Pérez, Wolf Steels, Jelle Huysentruyt, Bruno Verstraeten, Jessica Vetters, Tatyana Divert, et al. 2024. “Type 1 Immunity Enables Neonatal Thymic ILC1 Production.” SCIENCE ADVANCES 10 (3). https://doi.org/10.1126/sciadv.adh5520.
- Chicago author-date (all authors)
- Tougaard, Peter, Mario Ruiz Pérez, Wolf Steels, Jelle Huysentruyt, Bruno Verstraeten, Jessica Vetters, Tatyana Divert, Amanda Gonçalves, Ria Roelandt, Nozomi Takahashi, Sophie Janssens, Terkild B. Buus, Tom Taghon, Georges Leclercq, and Peter Vandenabeele. 2024. “Type 1 Immunity Enables Neonatal Thymic ILC1 Production.” SCIENCE ADVANCES 10 (3). doi:10.1126/sciadv.adh5520.
- Vancouver
- 1.Tougaard P, Ruiz Pérez M, Steels W, Huysentruyt J, Verstraeten B, Vetters J, et al. Type 1 immunity enables neonatal thymic ILC1 production. SCIENCE ADVANCES. 2024;10(3).
- IEEE
- [1]P. Tougaard et al., “Type 1 immunity enables neonatal thymic ILC1 production,” SCIENCE ADVANCES, vol. 10, no. 3, 2024.
@article{01HQWRBM7KWCVV58GW9MAMHRNB,
abstract = {{Acute thymic atrophy occurs following type 1 inflammatory conditions such as viral infection and sepsis, resulting in cell death and disruption of T cell development. However, the impact type 1 immunity has on thymic-resident innate lymphoid cells (ILCs) remains unclear. Single-cell RNA sequencing revealed neonatal thymic-resident type 1 ILCs (ILC1s) as a unique and immature subset compared to ILC1s in other primary lymphoid organs. Culturing murine neonatal thymic lobes with the type 1 cytokines interleukin-12 (IL-12) and IL-18 resulted in a rapid expansion and thymic egress of KLRG1(+)CXCR6(+) cytotoxic ILC1s. Live imaging showed the subcapsular thymic localization and exit of ILC1s following IL-12 + IL-18 stimulation. Similarly, murine cytomegalovirus infection in neonates resulted in thymic atrophy and subcapsular localization of thymic-resident ILC1s. Neonatal thymic grafting revealed that type 1 inflammation enhances the homing of cytokine-producing thymus-derived ILC1s to the liver and peritoneal cavity. Together, we show that type 1 immunity promotes the expansion and peripheral homing of thymic-derived ILC1s.}},
articleno = {{eadh5520}},
author = {{Tougaard, Peter and Ruiz Pérez, Mario and Steels, Wolf and Huysentruyt, Jelle and Verstraeten, Bruno and Vetters, Jessica and Divert, Tatyana and Gonçalves, Amanda and Roelandt, Ria and Takahashi, Nozomi and Janssens, Sophie and Buus, Terkild B. and Taghon, Tom and Leclercq, Georges and Vandenabeele, Peter}},
issn = {{2375-2548}},
journal = {{SCIENCE ADVANCES}},
language = {{eng}},
number = {{3}},
pages = {{17}},
title = {{Type 1 immunity enables neonatal thymic ILC1 production}},
url = {{http://doi.org/10.1126/sciadv.adh5520}},
volume = {{10}},
year = {{2024}},
}
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