Systemic Lupus Erythematosus (SLE) and Type I IFN

In recent years, the study of Systemic Lupus Erythematosus (SLE) patients has revealed a central role for Interferon alpha (IFN-α) in disease pathogenesis. Furthermore, endogenous nucleic acids and immune complexes (IC) activate Toll-Like Receptors (TLRs) and provide an amplification loop for Type I IFN production by plasmacytoid dendritic cells (pDCs) and for B cell activation in SLE. Indeed, a series of host factors have been recently described that modify self nucleic acids to gain entrance into endosomal compartments within pDCs, where they activate interferogenic TLR signaling. The unabated production of IFN-α induces the transcription of molecules that further contribute to amplify this pathogenic loop. Polymorphisms in genes controlling Type I IFN production or its downstream signaling pathway, such as IRF5, have been recently reported as conferring genetic susceptibility to SLE.

 

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Systemic Lupus Erythematosus and Type I Interferon

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