Apoptosis in systemic lupus erythematosus

Ibrahim Marai, Gisele Zandman-Goddard, Yehuda Sheonfeld

Research output: Contribution to journalReview articlepeer-review

2 Scopus citations

Abstract

In autoimmune diseases including systemic lupus erythematosus (SLE), the immune system attacks various autoantigens and causes damage in target organs. Recently, it was found that dead cells serve as a repertoire for autoantigens which can stimulate an autoimmune response in sensitive persons. The mechanisms which lead to induction and progress of apoptosis include extra-cellular stimuli, intra-cellular signals, and cleavage of proteins. During apoptosis, several events occur including migration of intra-cellular components to the cell membrane, removal of apoptotic cells by specific proteins and complement systems, and phagocytosis of apoptotic cells by macrophages. In recent years, evidence has accumulated that the autoimmune response can be initiated as a result of defects in apoptosis and/or removal of apoptotic material. In this article, the association of apoptosis to the pathogenesis of systemic lupus erythematosus is discussed.

Original languageHebrew
Pages (from-to)844-847+876
JournalHarefuah
Volume142
Issue number12
StatePublished - Dec 2003

Keywords

  • Apoptosis
  • Autoimmune lymphoproliferative syndrome
  • Systemic lupus erythematosus
  • TNFR-associated periodic syndrome

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