Table 2.

The mechanisms of exosomes in systemic lupus erythematosus pathogenesis

Exosome Source	Model	Mechanism	Ref.
Serum of SLE patients	PBMCs	Up-regulated the expression of IFN-α, TNF-α, IL-1β, and IL-6 in healthy peripheral blood mononuclear cells (PBMCs) in a TLR-dependent manner	(51)
Plasma of SLE patients		Exosome-delivered microRNAs promote IFN-α secretion by human plasmacytoid DCs via TLR7	(54)
Blood of SLE patients	SLE patients	Differently expressed exosomal miRNAs and proteins mainly enriched in pathways associated with inflammation and autophagy	(52)
Serum of SLE patients with or without lupus nephritis		MiR-21 and miR-155 were elevated in the serum of SLE patients compared to healthy controls, with even higher levels in SLE patients with LN	(53)
Serum of SLE patients		MiRNAs containing an IFN induction motif promoted activation, maturation, and survival of human plasmacytoid DCs via stimulating TLR7 expression	(55)
T cells of Lck-BPI Tg mice	C57BL/6J mice	Increased autoantibody levels, tissue IFN-γ levels, and induced hepatitis, nephritis, and arthritis in recipient mice	(56)
T cells of T-cell-specific BPI transgenic mice		Stimulated IL-1β production of macrophages and induced liver, kidney, and joint inflammatory responses	(57)