title: Type I interferon in systemic lupus erythematosus and other autoimmune diseases.
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.
authors.affiliation: Baylor Institute for Immmunology Research, 3434 Live Oak, Dallas, Texas 75204, USA. jacquesb@baylorhealth.edu
authors.forename: Jacques
authors.initials: J
authors.lastname: Banchereau
authors.forename: Virginia
authors.initials: V
authors.lastname: Pascual
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D007370:Interferon Type I / Q000502:physiology*; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D013577:Syndrome
chemical_list: D007370:Interferon Type I