Activated platelets and extracellular vesicles can stimulate neutrophils to undergo neutrophil extracellular trap (NET)osis, pDCs to produce IFNα, B cells to produce autoantibodies, regulatory T cells to downregulate FOXP3, and maturation of monocytes to APCs [111], all factors that can contribute to disease progression in SLE. Here, FOXP3 is linked to systemic lupus erythematosus.