[Pathophysiology of systemic lupus erythematosus]

Presse Med. 2007 May;36(5 Pt 2):825-34. doi: 10.1016/j.lpm.2006.11.017. Epub 2007 Jan 5.
[Article in French]

Abstract

Innate immunity is directly implicated in the pathophysiology of lupus through the dendritic cell system and the activation by immune complexes of some toll-like receptors (TLR). Interferon-alpha plays a key role in the pathophysiology of lupus and represents a promising target for immune therapy. Dendritic cells are activated and able to capture large quantities of nuclear antigen-containing bodies to stimulate specific adaptive immune response.

Publication types

  • Comparative Study
  • English Abstract
  • Review

MeSH terms

  • Adolescent
  • Adult
  • Animals
  • Antigen-Antibody Complex / immunology
  • Antigens, Nuclear / immunology
  • Apoptosis / physiology
  • Autoantigens / immunology
  • Autoimmunity / immunology
  • B-Lymphocytes
  • CD4-Positive T-Lymphocytes / immunology
  • CD8-Positive T-Lymphocytes / immunology
  • Child
  • Dendritic Cells / immunology
  • Dendritic Cells / physiology
  • Disease Models, Animal
  • Female
  • Humans
  • Interferon-alpha / physiology
  • Lupus Erythematosus, Systemic / immunology
  • Lupus Erythematosus, Systemic / physiopathology*
  • Male
  • Mice
  • Toll-Like Receptors / physiology

Substances

  • Antigen-Antibody Complex
  • Antigens, Nuclear
  • Autoantigens
  • Interferon-alpha
  • Toll-Like Receptors