Type 1 immunity enables neonatal thymic ILC1 production

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  • Peter Tougaard
  • Mario R. Pérez
  • Wolf Steels
  • Jelle Huysentruyt
  • Bruno Verstraeten
  • Jessica Vetters
  • Tatyana Divert
  • Amanda Gonçalves
  • Ria Roelandt
  • Nozomi Takahashi
  • Sophie Janssens
  • Buus, Terkild Brink
  • Tom Taghon
  • Georges Leclercq
  • Peter Vandenabeele

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.

Original languageEnglish
Article numbereadh5520
JournalScience Advances
Issue number3
Number of pages17
Publication statusPublished - 2024

ID: 380749102