TNF, apoptosis and autoimmunity: A common thread?

Bruce Beutler, Flavia Bazzoni

Research output: Contribution to journalArticle

73 Citations (Scopus)

Abstract

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
Volume24
Issue number2
DOIs
StatePublished - Jun 1998

Fingerprint

Autoimmunity
Tumor Necrosis Factor-alpha
Apoptosis
Autoimmune Diseases
Cytokines
Fas Ligand Protein
Crohn Disease
Rheumatoid Arthritis
Mutation

Keywords

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

ASJC Scopus subject areas

  • Molecular Biology
  • Molecular Medicine
  • Hematology

Cite this

TNF, apoptosis and autoimmunity : A common thread? / Beutler, Bruce; Bazzoni, Flavia.

In: Blood Cells, Molecules and Diseases, Vol. 24, No. 2, 06.1998, p. 216-230.

Research output: Contribution to journalArticle

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