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ZFP36L1 and ZFP36L2 cooperatively regulate thymic epithelial cell function to prevent early-onset thymic involution.

Pedro Ferreirinha1, Pedro M Rodrigues1, Francisco Sobral1

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Cell Death and Differentiation
|June 24, 2026
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Summary
This summary is machine-generated.

RNA-binding proteins ZFP36L1 and ZFP36L2 are crucial for maintaining thymic epithelial cell (TEC) differentiation and function. Their deficiency leads to early thymic aging and impaired T-cell development.

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Area of Science:

  • Immunology
  • Developmental Biology
  • Molecular Biology

Background:

  • The thymus is essential for T-cell maturation, but its function declines with age.
  • Thymic epithelial cells (TECs) are critical for T-cell development, with distinct cortical (c) and medullary (m) subsets.
  • The molecular regulation of TEC differentiation from progenitors is not fully understood.

Purpose of the Study:

  • To investigate the role of RNA-binding proteins ZFP36L1 and ZFP36L2 in TEC differentiation and thymic function.
  • To elucidate the molecular mechanisms by which ZFP36L1 and ZFP36L2 regulate the TEC microenvironment.

Main Methods:

  • Utilized dual conditional knockout (dcKO) and lineage-tracing mouse models.
  • Performed single-cell transcriptomics to analyze TEC populations and transcriptional programs.
  • Conducted fate-mapping analysis to trace TEC progenitor differentiation.

Main Results:

  • TEC-specific deletion of Zfp36l1 and Zfp36l2 caused early thymic hypoplasia and reduced TEC and thymocyte numbers.
  • Single-cell transcriptomics revealed altered TEC subset composition and metabolic gene dysregulation.
  • Fate-mapping showed disrupted differentiation trajectories from TEC progenitors to mature TECs.

Conclusions:

  • ZFP36L1 and ZFP36L2 cooperatively maintain TEC differentiation and thymic function.
  • Their deficiency impairs TEC development, leading to premature thymic involution.
  • These findings highlight a critical role for post-transcriptional regulation in sustaining thymic immunity.