1. Figure 2 Cellular contributions to the development of SLE
Figure 2 | Cellular contributions to the development of SLE. Neutrophils and apoptotic cells are at the apex of the cascade of pathogenetic mechanisms in systemic lupus erythematosus (SLE). They provide the critical ligands to drive expression of type I interferons (IFNs). Neutrophils represent a key inflammatory participant in organ damage; these cells also release neutrophil extracellular traps (NETs), a source of citrullinated peptide and nucleic acid antigens, via NETosis. Many cells produce type I IFNs, but plasmacytoid dendritic cells produce the highest levels of these cytokines. Apoptotic debris can also activate inflammatory cytokine expression which participates in the recruitment of cells into tissues. T cells and B cells both participate in autoreactivity, with B cells ultimately producing autoantibodies. T-cell production of IL-17 also contributes to organ infiltration by neutrophils. BAFF, B-cell activating factor; BAFF-R, BAFF receptor; CAMP, cathelicidin antimicrobial peptide; FcR, Fc receptor; MHC, major histocompatibility complex; TACI, transmembrane activator and cyclophilin ligand interactor; TLR, Toll-like receptor.
Tsokos, G. C. et al. (2016) New insights into the immunopathogenesis of systemic lupus erythematosus
Nat. Rev. Rheumatol. doi: /nrrheum