Type I Interferon in Systemic Lupus Erythematosus and Other Autoimmune Diseases

Baylor Institute for Immmunology Research, 3434 Live Oak, Dallas, Texas 75204, USA.
Immunity (Impact Factor: 19.75). 10/2006; 25(3):383-92. DOI: 10.1016/j.immuni.2006.08.010
Source: PubMed

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.

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