Apoptosis, subcellular particles, and autoimmunity

Amy M. Cline, Marko Radic

Research output: Contribution to journalArticle

74 Citations (Scopus)

Abstract

Firm evidence links the process of apoptosis to the induction of autoimmune disease. However, questions remain regarding the precise interactions of dying cells with the immune system. Genetic analyses indicate that deficiencies in serum proteins or receptors that mediate clearance of apoptotic cells increase the risk of autoimmunity. Moreover, administration of apoptotic cells to naive animals elicits transient autoimmune responses. Because known autoantigens are covalently modified and redistributed to cell surface blebs during the execution stage of apoptosis, increasing attention is being directed at this stage of programmed cell death, and researchers have identified a variety of autoantigens that are sequestered within blebs. However, blebs are merely a transition stage toward the complete cellular fragmentation, as blebs quickly convert into apoptotic bodies, subcellular particles (SCPs) of heterogeneous size, surface composition, and cargo. Because certain types of subcellular particles represent packets of highly enriched autoantigens, we propose that they are relevant to our understanding of autoimmunity.

Original languageEnglish (US)
Pages (from-to)175-182
Number of pages8
JournalClinical Immunology
Volume112
Issue number2
DOIs
StatePublished - Jan 1 2004

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Blister
Autoimmunity
Autoantigens
Apoptosis
Particle Size
Cell Communication
Autoimmune Diseases
Blood Proteins
Immune System
Cell Death
Research Personnel

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

Apoptosis, subcellular particles, and autoimmunity. / Cline, Amy M.; Radic, Marko.

In: Clinical Immunology, Vol. 112, No. 2, 01.01.2004, p. 175-182.

Research output: Contribution to journalArticle

Cline, Amy M. ; Radic, Marko. / Apoptosis, subcellular particles, and autoimmunity. In: Clinical Immunology. 2004 ; Vol. 112, No. 2. pp. 175-182.
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