Type 1 immunity enables neonatal thymic ILC1 production
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Type 1 immunity enables neonatal thymic ILC1 production. / Tougaard, Peter; Pérez, Mario R.; Steels, Wolf; Huysentruyt, Jelle; Verstraeten, Bruno; Vetters, Jessica; Divert, Tatyana; Gonçalves, Amanda; Roelandt, Ria; Takahashi, Nozomi; Janssens, Sophie; Buus, Terkild B.; Taghon, Tom; Leclercq, Georges; Vandenabeele, Peter.
In: Science Advances, Vol. 10, No. 3, eadh5520, 2024.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Type 1 immunity enables neonatal thymic ILC1 production
AU - Tougaard, Peter
AU - Pérez, Mario R.
AU - Steels, Wolf
AU - Huysentruyt, Jelle
AU - Verstraeten, Bruno
AU - Vetters, Jessica
AU - Divert, Tatyana
AU - Gonçalves, Amanda
AU - Roelandt, Ria
AU - Takahashi, Nozomi
AU - Janssens, Sophie
AU - Buus, Terkild B.
AU - Taghon, Tom
AU - Leclercq, Georges
AU - Vandenabeele, Peter
PY - 2024
Y1 - 2024
N2 - 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.
AB - 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.
U2 - 10.1126/sciadv.adh5520
DO - 10.1126/sciadv.adh5520
M3 - Journal article
C2 - 38232171
AN - SCOPUS:85182793581
VL - 10
JO - Science advances
JF - Science advances
SN - 2375-2548
IS - 3
M1 - eadh5520
ER -
ID: 380749102