CD95-mediated apoptosis in vivo involves acid sphingomyelinase Academic Article uri icon


MeSH Major

  • Antigens, CD95
  • Apoptosis
  • Sphingomyelin Phosphodiesterase


  • Acid sphingomyelinase (ASM) is reported to have an essential function in stress-induced apoptosis although the physiological function of ASM in receptor-triggered apoptosis is unknown. Here, we delineate a pivotal role for ASM in CD95-triggered apoptosis of peripheral lymphocytes or hepatocytes in vivo. We employed intravenous injection of anti-CD4 antibodies or phytohemagglutinin that was previously shown to result in apoptosis of peripheral blood lymphocytes or hepatocytes via the endogenous CD95/CD95 ligand system. Our results demonstrate a high susceptibility in normal mice whereas ASM knock-out mice fail to immunodeplete T cells or develop autoimmune-like hepatitis. Likewise, ASM-deficient mice or hepatocytes and splenocytes ex vivo manifest resistance to anti-CD95 treatment. These results provide in vivo evidence for an important physiological function of ASM in CD95-induced apoptosis.

publication date

  • September 2000



  • Academic Article



  • eng

Digital Object Identifier (DOI)

  • 10.1074/jbc.M002957200

PubMed ID

  • 10867001

Additional Document Info

start page

  • 27316

end page

  • 23


  • 275


  • 35