Type I Interferon in Systemic Lupus Erythematosus and Other Autoimmune Diseases Review uri icon

Overview

MeSH Major

  • Interferon Type I
  • Lupus Erythematosus, Systemic

abstract

  • Different genetic alterations may lead to type I interferon (IFN) overproduction in human systemic lupus erythematosus (SLE). The increased bioavailability of type I IFN contributes to peripheral tolerance breakdown through the activation of immature myeloid dendritic cells (mDCs). IFN-matured mDCs activate autoreactive T cells. These cells, together with plasmacytoid DCs, help expand autoreactive B cells. IFN-matured DCs also activate cytotoxic CD8+ T cells, possibly increasing apoptotic cell availability. The capture of apoptotic cells by mDCs and of nucleic acid-containing immune complexes by plasmacytoid DCs and B cells amplifies the autoimmune reaction leading to disease manifestations. Genetic alterations in lineages other than B cells might explain other autoimmune syndromes where type I IFNs appear to be involved.

publication date

  • September 2006

Research

keywords

  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1016/j.immuni.2006.08.010

PubMed ID

  • 16979570

Additional Document Info

start page

  • 383

end page

  • 92

volume

  • 25

number

  • 3