Fas/Fas ligand-mediated apoptosis of murine Langerhans cells

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Published on: March 6, 2010

T Kawamura1, M Azuma, N Kayagaki

  • 1Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan. kawamura@box-k.nih.gov

Journal of Dermatological Science
|February 16, 2000
PubMed

Insights

Murine epidermal Langerhans cells (LC) express Fas (CD95), which is upregulated by IFN-gamma. LC undergo Fas-mediated apoptosis when treated with both Fas ligand (FasL) and IFN-gamma, suggesting a mechanism for regulating skin immunity.

Area of Science:

  • Immunology
  • Dermatology
  • Cell Biology

Background:

  • Epidermal Langerhans cells (LC) are key antigen-presenting cells (APC) initiating skin immune responses.
  • The Fas/Fas ligand (FasL) pathway is critical for regulating peripheral immunity.
  • Mechanisms controlling LC elimination remain largely unknown.

Purpose of the Study:

  • To investigate the role of the Fas pathway in epidermal Langerhans cell apoptosis.
  • To determine if IFN-gamma influences Fas expression and apoptosis susceptibility in LC.

Main Methods:

  • Murine epidermal LC were cultured in vitro.
  • Fas (CD95) expression was analyzed.
  • Apoptosis was induced using recombinant soluble Fas ligand (FasL) and/or IFN-gamma.

Main Results:

  • Murine epidermal LC constitutively express Fas (CD95).
  • IFN-gamma up-regulates Fas expression on LC.
  • LC undergo apoptosis upon combined treatment with FasL and IFN-gamma, but not FasL alone.

Conclusions:

  • LC susceptibility to Fas-mediated apoptosis is enhanced by IFN-gamma-induced Fas upregulation.
  • LC elimination via this pathway may prevent excessive cutaneous inflammation.
  • This highlights a novel mechanism for immune homeostasis in the skin.

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