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Effector differentiation downstream of lineage commitment in ILC1s is driven by Hobit across tissues
Christin Friedrich1, Renske L R E Taggenbrock2, Rémi Doucet-Ladevèze1
1Würzburg Institute of Systems Immunology (WüSI), Max Planck Research Group at the Julius-Maximilians-Universität Würzburg, Würzburg, Germany.
Nature Immunology
|August 31, 2021
Summary
Innate lymphoid cells (ILCs) develop effector functions through a conserved pathway. Early TCF-1 high ILC1s mature into tissue-specific cells, losing expansion potential and gaining effector function via Hobit.
Area of Science:
- Immunology
- Cell Biology
- Developmental Biology
Background:
- Innate lymphoid cells (ILCs) are crucial for immunity and tissue health.
- The mechanisms of ILC effector function acquisition and organ-specific differences remain unclear.
Purpose of the Study:
- To investigate the differentiation pathways of ILC1s.
- To determine if ILC differentiation mechanisms are conserved across different organs.
Main Methods:
- Multiplexed single-cell mRNA sequencing was used to analyze ILC populations.
- Key transcription factors (TCF-1, Hobit) and cell surface markers (cKit, CD127) were assessed.
Main Results:
- Early ILC1 differentiation stages (cKit+, CD127hi, TCF-1hi) were identified across organs.
- Differentiating ILC1s showed a stepwise loss of TCF-1 and expansion potential, with increased effector molecule expression.
- The transcription factor Hobit was induced in TCF-1hi ILC1s and essential for effector differentiation.
Conclusions:
- ILC1 differentiation involves sequential commitment and effector function acquisition, conserved across tissues.
- ILC1s emerge as TCF-1hi cells and adopt organ-specific phenotypes via a Hobit-dependent pathway influenced by local cues.
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