Apoptosis and systemic autoimmunity: The dendritic cell connection

P. Rovere, F. Fazzini, M. G. Sabbadini, A. A. Manfredi

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Much effort has been devoted in recent years to the events linking recognition and disposal of apoptotic cells to sustained immunity towards the antigens they contain. Programmed death via apoptosis indeed provides most of the raw material the immune system exploits to establish self tolerance, i.e. to learn how to distinguish between self constituents and foreign antigens, belonging to invading pathogens. In parallel, events occurring during cell death may enable a restricted array of molecules endowed with diverse structure, function and intracellular distribution to satisfy the requirement to evoke and maintain autoimmune responses. Dendritic cells (DCs), the most potent antigen presenting cells, appear to play a crucial role. Here we will discuss some of the constrains regulating the access of dying cells' antigens to DCs, as well as censorship mechanisms that prevent their maturation and the full explication of their antigen presenting function.

Original languageEnglish
Pages (from-to)229-236
Number of pages8
JournalEuropean journal of histochemistry : EJH
Volume44
Issue number3
Publication statusPublished - 2000

Fingerprint

autoimmunity
dendritic cells
Autoimmunity
Dendritic Cells
apoptosis
Apoptosis
antigens
Antigens
Self Tolerance
antigen-presenting cells
Antigen-Presenting Cells
immune system
raw materials
cell death
Immune System
Immunity
Cell Death
immunity
cells
death

Keywords

  • Antigen presentation
  • Apoptosis
  • Autoimmunity
  • Dendritic cells
  • Systemic lupus erythematosus

ASJC Scopus subject areas

  • Cell Biology
  • Anatomy
  • Animal Science and Zoology
  • Developmental Biology

Cite this

Apoptosis and systemic autoimmunity : The dendritic cell connection. / Rovere, P.; Fazzini, F.; Sabbadini, M. G.; Manfredi, A. A.

In: European journal of histochemistry : EJH, Vol. 44, No. 3, 2000, p. 229-236.

Research output: Contribution to journalArticle

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