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T-bet and RORα control lymph node formation by regulating embryonic innate lymphoid cell differentiation
Christina Stehle1, Timo Rückert1, Rémi Fiancette2
1Innate Immunity, German Rheumatism Research Centre-a Leibniz Institute, Berlin, Germany.
Nature Immunology
|September 24, 2021
Summary
T-bet deficiency rescues lymph node formation in mice lacking RORγt. This occurs because T-bet influences fetal innate lymphoid cell differentiation, promoting lymphoid tissue inducer cell accumulation.
Area of Science:
- Immunology
- Developmental Biology
- Cell Biology
Background:
- Group 3 innate lymphoid cells (ILC3) expressing RORγt are essential for lymphoid tissue formation during embryogenesis.
- RORγt-deficient mice lack ILC3 and lymphoid structures like lymph nodes (LN).
- The role of T-bet in fetal ILC3 and LN development is unknown, though it impacts postnatal ILC3 function.
Purpose of the Study:
- To investigate the role of T-bet in embryonic ILC3 development and lymph node formation.
- To determine if T-bet influences the development of RORγt-deficient fetal ILCs and lymph node structures.
Main Methods:
- Utilized multiple mouse models, including RORγt-deficient mice.
- Performed single-cell analyses on fetal ILCs and ILC progenitors (ILCP).
- Investigated the impact of T-bet deficiency on fetal ILC differentiation and ILCP accumulation.
Main Results:
- T-bet plays a critical role during embryogenesis in regulating ILC3 differentiation and LN formation.
- T-bet deficiency rescued lymph node formation in RORγt-deficient mice.
- T-bet deletion promoted the accumulation of PLZFhi ILCP expressing lymphoid tissue inducer molecules, dependent on RORα.
Conclusions:
- T-bet unexpectedly functions during embryonic development to regulate ILC differentiation and LN formation.
- RORα is involved in the T-bet-mediated regulation of fetal ILCP.
- RORγt is essential for counteracting the suppressive effects of T-bet on lymph node development.
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