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Medullary TEC-derived FGF21 (fibroblast growth factor 21) rejuvenates the aging thymus by promoting mTOR signaling in cTECs. This enhances T-cell function and self-tolerance, offering therapeutic potential for age-related immune decline.

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Area of Science:

  • Immunology
  • Aging Research
  • Cell Biology

Background:

  • Age-associated thymic atrophy leads to reduced T-cell function and impaired self-tolerance.
  • Cortical thymic epithelial cells (cTECs) are crucial for T-cell development and are affected by thymic aging.
  • mTOR signaling, downstream of medullary TEC (mTEC)-derived factors, is implicated in cTEC maintenance.

Purpose of the Study:

  • To investigate the role of mTEC-derived FGF21 in regulating thymus size and function during aging.
  • To determine the impact of FGF21 on mTOR signaling pathways within cTECs.
  • To assess the effects of FGF21 on T-cell responsiveness and autoimmunity in aged mice.

Main Methods:

  • Generated a knock-in mouse model expressing FGF21 and mCherry in mTECs.
  • Administered the mTOR inhibitor rapamycin to assess its effect on FGF21-mediated signaling.
  • Evaluated thymus size, cTEC maintenance, T-cell responses to viral infection, and indicators of peripheral autoimmunity.

Main Results:

  • mTEC-derived FGF21 promoted distinct mTORC1 and mTORC2 signaling patterns in cTECs.
  • FGF21 overexpression led to increased thymus and cTEC size and improved maintenance.
  • Enhanced T-cell responsiveness to viral infection and reduced autoimmunity were observed in older mice.
  • Rapamycin treatment abrogated the effects of FGF21 on thymus size and mTOR signaling.

Conclusions:

  • Paracrine FGF21 signaling is a key regulator of thymus size and function across the lifespan.
  • FGF21 influences T-cell immunity and self-tolerance by modulating mTOR signaling in cTECs.
  • Targeting FGF21-mTOR pathways presents a potential therapeutic strategy for age-related immune dysfunction.