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Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
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Sonic Hedgehog regulates thymic epithelial cell differentiation.

José Ignacio Saldaña1, Anisha Solanki1, Ching-In Lau1

  • 1Immunobiology Section, UCL Institute of Child Health, 30 Guilford Street London WC1N 1EH, UK.

Journal of Autoimmunity
|January 19, 2016
PubMed
Summary
This summary is machine-generated.

Sonic Hedgehog (Shh) signaling is crucial for thymic epithelial cell (TEC) development and differentiation. This study reveals Shh

Keywords:
MHCIIMorphogenSonic hedgehogT cellThymic epitheliumcTECmTEC

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Area of Science:

  • Immunology
  • Developmental Biology
  • Cell Biology

Background:

  • The Sonic Hedgehog (Shh) signaling pathway plays a role in T cell development within the thymus.
  • Thymic epithelial cells (TECs) express components of the Hedgehog (Hh) signaling pathway, indicating its potential role in TEC regulation.
  • Active Hh-dependent transcription is confirmed in fetal and adult TECs using a Gli Binding Site-green fluorescence protein (GFP) reporter mouse.

Purpose of the Study:

  • To investigate the influence of Sonic Hedgehog (Shh) on thymic epithelial cell (TEC) development and differentiation.
  • To elucidate the role of Shh in regulating TEC numbers, proportions of medullary and cortical TECs, and MHC Class II expression.
  • To determine the impact of Shh signaling on T cell development originating from TECs.

Main Methods:

  • Analysis of Shh-deficient fetal thymus organ cultures (FTOC) to assess TEC differentiation and numbers.
  • Investigation of Gli3-deficient thymus to understand the effects of altered Hh signaling.
  • Neutralization of endogenous Hh proteins in wild-type (WT) FTOC.
  • Conditional deletion of Shh from TECs in adult thymus.
  • Treatment of human thymus explants with recombinant Shh or anti-Shh antibody.

Main Results:

  • Shh deficiency in FTOC leads to reduced TEC numbers, a decreased proportion of medullary TECs, and increased MHC Class II expression on both cortical and medullary TECs.
  • Gli3 deficiency results in increased TEC numbers but decreased MHC Class II expression on TECs.
  • Neutralization of Hh in WT FTOC reduces TEC numbers and mature medullary TECs while increasing MHC Class II expression.
  • Conditional Shh deletion in adult TECs alters TEC differentiation, reduces TEC numbers and mature medullary TECs, and increases MHC Class II expression on medullary TECs.
  • Shh signaling in TECs regulates the differentiation of mature CD4 and CD8 single positive thymocytes.
  • Hedgehog pathway involvement in DP to SP T cell differentiation is observed in human thymus explants.

Conclusions:

  • Sonic Hedgehog (Shh) is essential for normal thymic epithelial cell (TEC) differentiation and homeostasis.
  • Shh signaling directly influences the balance between cortical and medullary TEC populations and their maturation.
  • TEC-derived Shh signaling plays a critical regulatory role in T cell development within the thymus, including in humans.