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Single-cell RNA-seq and computational analysis using temporal mixture modelling resolves Th1/Tfh fate bifurcation in
Tapio Lönnberg1, Valentine Svensson2, Kylie R James3
1European Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI), Wellcome Genome Campus, Hinxton, Cambridge, UK; Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, UK.
This study maps T helper cell differentiation during malaria infection, revealing Galectin-1 promotes Th1 cell development and inflammatory monocytes guide precursor cells towards Th1 fates.
Area of Science:
- Immunology
- Computational Biology
- Genomics
Background:
- T helper cell differentiation is vital for adaptive immunity.
- Dissecting T cell heterogeneity and transcriptional programs in vivo remains challenging.
Purpose of the Study:
- To reconstruct developmental trajectories of Th1 and Tfh cells during Plasmodium infection.
- To identify factors influencing Th1/Tfh fate commitment.
- To develop computational tools for analyzing cell differentiation.
Main Methods:
- Single-cell transcriptomics
- Computational analysis using GPfates (Gaussian processes model)
- Tracking clonality via endogenous TCR sequences
Main Results:
- Th1/Tfh bifurcation confirmed at population and single-clone levels.
- Galectin-1 identified as a T-cell intrinsic factor promoting Th1 differentiation.
- Inflammatory monocytes were found to direct precursor T cells towards Th1 fates.
Conclusions:
- GPfates provides a novel framework for modeling multi-fate cell differentiation.
- www.PlasmoTH.org offers a resource for discovering novel factors in T helper cell fate commitment.
- The study elucidates key mechanisms governing Th1 and Tfh cell differentiation during infection.
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