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Previous studies have shown that increased levels of anti-neutrophil cytoplasmic antibodies (ANCAs) in SLE patients serum suggest an impaired clearance mechanism for neutrophil debris, a significant source of self-antigens ( Apoptotic cell bodies: Lymphocytes from SLE patients frequently experience accelerated apoptosis, releasing nuclear antigens like nucleosomes into the extracellular space, which can then trigger immune responses and autoantibody formation ( Type-I IFN: Type-I IFN facilitates dendritic cell (DC) maturation, enhances autoimmune T cell survival, and activates autoantibody-producing B cells, primarily through sustained IFN- production, autophosphorylation, and activation of the IFN- receptor (IFNAR)-associated Janus kinases (JAKs) and signal transducers and activators of transcription (STATs) ( Figure 2 4 Current and potential treatment for SLE To date, there is no definitive strategy for the treatment of SLE that can replace traditional therapies ( Figure 3 )

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