TNF, apoptosis and autoimmunity: A common thread?

Bruce Beutler, Flavia Bazzoni

Research output: Contribution to journalArticlepeer-review

79 Scopus citations


A subset of cytokine mediators belonging to the tumor necrosis factor (TNF) family cause apoptosis, acting through receptors and signaling pathways that have recently come to light. Further, at least one autoimmune disease results from a defined defect of apoptosis (mutations of the Fas ligand or its receptor). It is offered that many, and perhaps most autoimmune diseases may result from primary defects of apoptosis. Such defects may cause reflexive overproduction of TNF and other pro-apoptotic cytokines. The collateral damage produced by these mediators may be of pathogenetic importance in complex autoimmune disorders such as rheumatoid arthritis and Crohn disease, wherein TNF blockade is known to have ameliorative effects.

Original languageEnglish (US)
Pages (from-to)216-230
Number of pages15
JournalBlood Cells, Molecules and Diseases
Issue number2
StatePublished - Jun 1998


  • Autoimmunity
  • Cytokine
  • Fas ligand
  • Receptor
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Hematology
  • Cell Biology


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