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To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.

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FOXN1 mutation abrogates prenatal T-cell development in humans.

I Vigliano1, M Gorrese, A Fusco

  • 1Department of Pediatrics, 'Federico II' University, Via Pansini, 5, Naples 80131, Italy. pignata@unina.it

Journal of Medical Genetics
|April 22, 2011
PubMed
Summary

The transcription factor FOXN1 is essential for human T cell development in the womb. Its absence blocks CD4(+) T cell maturation and impairs CD8(+) cells, suggesting extrathymic origins for some lymphocytes.

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Area of Science:

  • Immunology
  • Developmental Biology
  • Genetics

Background:

  • The transcription factor FOXN1 plays a key role in thymic and skin epithelial cell differentiation.
  • Mutations in FOXN1 cause the Nude/Severe Combined Immunodeficiency (SCID) phenotype.
  • A unique opportunity arose to study T cell development in a FOXN1(-/-) human fetus.

Purpose of the Study:

  • To investigate the role of FOXN1 in human in utero T cell development.
  • To analyze T cell maturation and T cell receptor (TCR) diversity in a FOXN1-deficient fetus.

Main Methods:

  • Analysis of T cell populations (CD4+, CD8+) in a FOXN1(-/-) fetus.
  • Evaluation of T cell receptor (TCR) variable-domain β-chain (Vβ) family usage.
  • Assessment of CD3 and TCRγδ expression on T lymphocytes.

Main Results:

  • Complete blockage of CD4(+) T cell maturation was observed.
  • Severe impairment of CD8(+) T cell development occurred.
  • TCR diversity generation was present but impaired; some non-functional CD8(+) cells with TCRγδ were found.

Conclusions:

  • FOXN1 is critical for T cell development during human gestation.
  • The presence of limited CD8(+) cells suggests a FOXN1-independent pathway for lymphopoiesis, potentially extrathymic.