| First Author | Tougaard P | Year | 2024 |
| Journal | Sci Adv | Volume | 10 |
| Issue | 3 | Pages | eadh5520 |
| PubMed ID | 38232171 | Mgi Jnum | J:344475 |
| Mgi Id | MGI:7575247 | Doi | 10.1126/sciadv.adh5520 |
| Citation | Tougaard P, et al. (2024) Type 1 immunity enables neonatal thymic ILC1 production. Sci Adv 10(3):eadh5520 |
| abstractText | 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. |
