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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: Semin Nephrol. 2015 Sep;35(5):396–409. doi: 10.1016/j.semnephrol.2015.08.002

Figure 1.

Figure 1

Innate immunity processes contribute to lupus nephritis. A. Enhanced programmed cell death (PCD) coupled with decreased clearance of PCD debris results in the availability of nuclear autoantigens, including nucleosomes, nuclear particles, RNA, and DNA. B. Intracellular RNA (RIGI-I and MDA5) and DNA (cGAS) sensors interact with RNA, DNA, and nuclear particles. C. Nuclear antigens are opsonized by antibodies, complement, pentraxins, and/or collectins (the latter two then interact with complement components), which then interact with Fc (antibody) or complement (CR) receptors to bring antigens into phagocytic endosomes, where RNA and DNA can interact with the TLR receptors TLR3, TLR7 and TLR9, respectively. The helicase (B) and Opsonin/TLR (C) pathways result in prolonged immune cell survival and secretion of pro-inflammatory cytokines. These include Type I IFNs, which then engage the Type I IFN receptor (D). Activation of the Type I IFN receptor results in the production of transcription factors, cytokines, and receptors that prolong and amplify the immune response.

*Genes/molecules with genetic variants associated with lupus nephritis