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Updated: Jun 16, 2026

Evaluation of T Follicular Helper Cells and Germinal Center Response During Influenza A Virus Infection in Mice
Published on: June 27, 2020
NFAT pulls the strings during CD4+ T helper cell effector functions.
Natascha Hermann-Kleiter1, Gottfried Baier
1Department for Medical Genetics, Molecular and Clinical Pharmacology, Medical University Innsbruck, Innsbruck, Austria. natascha.kleiter@i-med.ac.at
Nuclear Factor of Activated T cells (NFAT) transcription factors are crucial for CD4(+) T helper cell differentiation and function. They partner with other factors to regulate gene expression, influencing immune responses.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Nuclear Factor of Activated T cells (NFAT) is a calcium-dependent transcription factor family vital for T-cell immune responses.
- NFAT proteins exhibit weak DNA-binding, necessitating cooperation with other transcription factors at composite gene promoter sites.
Purpose of the Study:
- To review the critical role of NFAT interactions in CD4(+) T helper cell differentiation and effector functions.
- To elucidate the established transcriptional partners and functional outcomes of NFAT signaling in T helper cell subsets.
Main Methods:
- Literature review focusing on NFAT's role in T-cell activation and differentiation.
- Analysis of NFAT's transcriptional regulation of lineage-specific transcription factors (T-bet, Gata3, RORgammat, Foxp3).
- Examination of NFAT's control over signature cytokines and their receptors.
Main Results:
- NFAT is essential for inducing genetic programs that guide CD4(+) T helper subset differentiation (Th1, Th2, Th17, iTregs).
- NFAT regulates key transcription factors like T-bet, Gata3, RORgammat, and Foxp3.
- NFAT controls the expression of critical cytokines and cytokine receptors involved in T helper cell function.
Conclusions:
- NFAT integrates T-cell receptor signaling with other immune receptor pathways to determine T helper cell differentiation and function.
- Understanding NFAT interactions is crucial for comprehending effector responses in clinically relevant CD4(+) T helper subsets.
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