The innate immune system in SLE: type I interferons and dendritic cells

Lupus. 2008 May;17(5):394-9. doi: 10.1177/0961203308090020.

Abstract

Patients with systemic lupus erythematosus (SLE) have an increased expression of type I interferon (IFN) regulated genes because of a continuous production of IFN-alpha. The cellular and molecular background to this IFN-alpha production has started to be elucidated during the last years, as well as the consequences for the innate and adaptive immune systems. Plasmacytoid dendritic cells (pDC) activated by immune complexes containing nucleic acids secrete type I IFN in SLE. Type I IFN causes differentiation of monocytes to myeloid-derived dendritic cell (mDC) and activation of autoreactive T and B cells. A new therapeutic option in patients with SLE is, therefore, inhibition of IFN-alpha, and recent data from a phase I clinical trial suggests that administration of neutralizing monoclonal antibodies against anti-IFN-alpha can ameliorate disease activity.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptation, Biological / immunology
  • Animals
  • Dendritic Cells / immunology*
  • Humans
  • Immune System / immunology*
  • Immunity, Innate / immunology*
  • Interferon Type I / immunology*
  • Lupus Erythematosus, Systemic / etiology
  • Lupus Erythematosus, Systemic / immunology*

Substances

  • Interferon Type I