Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the overactivation of T cells and production of plenty of autoantibodies by activated B cells. Recent studies have shown that the pathogenesis of SLE is associated with gene-environment interactions. Dendritic cells (DCs) are known as the strongest antigen-presenting cells in human body, playing an important role in immune surveillance, immune defense and immune homeostasis, and are a key factor in innate and adaptive immunity. Myeloid and plasmacytoid DCs, two major DC subsets in human blood, both play important roles in the pathogenesis of SLE. Myeloid DCs can be activated through the mediation of apoptotic cells, and plasmacytoid DCs can express Toll-like receptors (TLRs) and secrete interferon-α. Moreover, DCs participate in the pathogenesis of SLE by acting on downstream immune responses and post-transcriptional regulations via microRNAs. Key words: Lupus erythematosus, systemic; Dendritic cells; MicroRNAs; Immunity; Autoantibodies

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