Fig. 1.

Disturbed immune system in SLE. Nuclear particles activate Toll like receptors (TLR) on antigen-presenting cells, mainly dendritic cells and promote their maturation. Persistent activation of dendritic cells induces T cell activation and proliferation. Activated T cells then lead to mature autoreactive B cells. Furthermore, ribonucleoprotein and U1snRNP can induce type I IFN secretion by pDCs in SLE, which promotes the differentiation of activated B cells into plasmablasts and antibody-secreting plasma cells. Autoantibodies can bind to nuclear antigens, form immune complex and activate innate immune cells, which is a positive feedback loop and amplifies the pathogenic processes in SLE.