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NFATc1 induction by an intronic enhancer restricts NKT γδ cell formation.

Sabrina Giampaolo1, Cristina M Chiarolla1, Konrad Knöpper2

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Removing the transcription factor NFATc1 during thymocyte development increases γδ T cells, including natural killer T (NKT) γδ cells. This process relies on the enhancer E2 for NFATc1

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Area of Science:

  • Immunology
  • Developmental Biology
  • Molecular Biology

Background:

  • T cell receptor (TCR) signaling is crucial for T cell development in the thymus.
  • NFATc1 is a key transcription factor in T cell activation and differentiation.
  • γδ T cells and αβ T cells are distinct lineages of T lymphocytes with different functions.

Purpose of the Study:

  • To investigate the role of NFATc1 in the development of γδ T cells and NKT γδ cells.
  • To identify regulatory elements controlling NFATc1 expression during thymocyte development.

Main Methods:

  • Genetic ablation of NFATc1 or its isoforms in thymocytes.
  • Flow cytometry to analyze thymocyte populations.
  • Analysis of gene expression and regulatory elements (enhancer E2, promoter P1).

Main Results:

  • Ablation of NFATc1 during double-negative (DN) stages significantly increased γδ thymocytes, while αβ thymocyte development was unaffected.
  • The resulting γδ thymocytes showed increased promyelocytic leukemia zinc-finger factor (PLZF) and an NKT γδ cell phenotype with enhanced survival.
  • NFATc1's suppressive function on NKT γδ cell development depends on the enhancer E2 and its role in inducible NFATc1 expression via promoter P1.
  • Enhancer E2 translates strong γδ TCR signals into inducible NFATc1 expression, controlling NKT γδ cell numbers.

Conclusions:

  • NFATc1 acts as a negative regulator of NKT γδ cell development in the thymus.
  • The enhancer E2 and promoter P1 are critical for regulating NFATc1's role in controlling NKT γδ cell populations.
  • Understanding these regulatory mechanisms provides insights into T cell lineage commitment and immune homeostasis.