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The cellular prion protein modulates phagocytosis and inflammatory response

Cecília J G de Almeida1, Luciana B Chiarini, Juliane Pereira da Silva

  • 1Instituto de Biofísica da UFRJ, Rio de Janeiro, RJ, Brasil. rlinden@biof.ufrj.br

Journal of Leukocyte Biology
|November 13, 2004
PubMed

Insights

The cellular prion protein (PrPc) regulates macrophage phagocytosis. Removing PrPc enhances the clearance of apoptotic cells and particles, impacting immune responses and prion disease pathogenesis.

Area of Science:

  • Immunology
  • Neuroscience
  • Cell Biology

Background:

  • Cellular prion protein (PrPc) is a GPI-anchored glycoprotein abundant in the central nervous system and immune cells.
  • Its role in cellular functions, particularly phagocytosis, remains largely unexplored.

Purpose of the Study:

  • To investigate the function of PrPc in the phagocytosis of apoptotic cells and other particles.
  • To elucidate the role of PrPc in immune cell activity and its implications for prion diseases.

Main Methods:

  • In vitro phagocytosis assays using macrophages from PrPc knockout (Prnp gene deletion) and wild-type mice.
  • In situ detection of phagocytosis in retinal tissues.
  • In vivo assays of acute peritonitis to assess particle clearance and leukocyte recruitment.

Main Results:

  • Macrophages lacking PrPc exhibited significantly higher phagocytic rates compared to wild-type macrophages.
  • Depletion of GPI-anchored proteins from wild-type macrophages mimicked the enhanced phagocytosis observed in knockout cells.
  • Augmented phagocytosis of apoptotic bodies and zymosan particles was observed in knockout mice, both in situ and in vivo.
  • Leukocyte recruitment patterns were altered in PrPc knockout mice.

Conclusions:

  • PrPc plays a modulatory role in phagocytosis, both in vitro and in vivo.
  • The findings suggest PrPc influences macrophage function and may be relevant to the pathogenesis of prion diseases.
  • This study reveals a novel function for PrPc in cellular clearance mechanisms.

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