Inhibition of lupus by genetic alteration of the interferon-alpha/beta receptor - PubMed (original) (raw)

Review

Inhibition of lupus by genetic alteration of the interferon-alpha/beta receptor

Dwight H Kono et al. Autoimmunity. 2003 Dec.

Free article

Abstract

Type I interferons (IFN-alphabeta) are immunoregulatory cytokines that promote both innate and adaptive immune responses. Although they have been implicated in human SLE, recent studies in mice have helped solidify this connection. By using lupus-prone mice with knockout of the IFN-alphabeta receptor, we and others have documented that lack of IFN-alphabeta leads to a marked reduction in disease manifestations, including autoantibody production, target organ damage and mortality. Furthermore, IFN-alphabeta was found to potentially contribute to several levels of disease pathogenesis. These included the differentiation and activation of dendritic cells, the activation and proliferation of T cells, T cell survival and the activation and survival of autoantibody-producing B cells. These findings strongly support the targeting of IFN-alphabeta in SLE and suggest that definition of the specific pathways critical for disease induction will be important for optimal intervention.

PubMed Disclaimer

Similar articles

Cited by

Publication types

MeSH terms

Substances

LinkOut - more resources