Type 1 immunity enables neonatal thymic ILC1 production.
Peter Tougaard1,2, Mario Ruiz Pérez1,2, Wolf Steels1,2
1Cell death and Inflammation Unit, VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Science Advances
|January 17, 2024
Summary
Type 1 inflammation drives the expansion and migration of unique neonatal thymic innate lymphoid cells (ILCs). These cytotoxic ILC1s relocate from the thymus to other organs, impacting immune responses.
Area of Science:
- Immunology
- Innate Immunity
- Developmental Immunology
Background:
- Acute thymic atrophy is linked to type 1 inflammatory conditions, affecting T cell development.
- The role of type 1 immunity in thymic-resident innate lymphoid cells (ILCs) is not well understood.
Purpose of the Study:
- To investigate the impact of type 1 immunity on neonatal thymic-resident ILCs.
- To characterize the unique subset of neonatal thymic ILC1s.
Main Methods:
- Single-cell RNA sequencing of neonatal thymic ILCs.
- In vitro culture of murine neonatal thymic lobes with IL-12 and IL-18.
- Live imaging of ILC1 localization and egress.
- Murine cytomegalovirus infection model.
- Neonatal thymic grafting experiments.
Main Results:
- Neonatal thymic ILC1s represent a unique, immature subset.
- IL-12 and IL-18 stimulation promote rapid expansion and egress of cytotoxic KLRG1+CXCR6+ ILC1s.
- Type 1 inflammation, including viral infection, induces thymic atrophy and subcapsular ILC1 localization.
- Thymus-derived ILC1s exhibit enhanced homing to the liver and peritoneal cavity.
Conclusions:
- Type 1 immunity significantly influences thymic-resident ILC populations.
- Neonatal thymic ILC1s are expanded and directed to peripheral tissues by type 1 inflammation.
- These findings reveal a novel mechanism for thymus-derived ILC1s in type 1 immune responses.
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