The Biology of Dendritic Cells in the Context of Autoimmunity

Abstract

Systemic lupus erythematosus (SLE) is a complex autoimmune disease that affects at least five million people worldwide. An increased expression of type I interferon (IFN) regulated genes is a hallmark of SLE, but the precise etiology of SLE initiation and flares is poorly understood. Because plasmacytoid dendritic cells (pDCs) are the primary type I IFN producers, their role in SLE has long been suspected, with murine pDC depletion models successfully delaying the progression of murine lupus-like disease. However, the mechanism behind how exactly how pDCs contribute to lupus autoimmunity is unknown, contributing to the current dearth lack of disease modifying treatments; current treatments only succeed in suppressing symptoms, and do not halt disease progression. In this study, we take a multifactorial approach to understanding the biology of pDCs in the context of lupus autoimmunity. Although the exact etiology of lupus is unknown, infections are an important environmental trigger for