1. Figure 2 Cell-mediated disease mechanisms of lupus nephritis
Figure 2 | Cell-mediated disease mechanisms of lupus nephritis. The sensing of immunostimulatory nucleic acids by dendritic cells drives B lymphocyte and T lymphocyte activation and the production of autoantibodies and autoantigen-specific T cells, leading to glomerular endothelium, podocyte, tubulointerstitial and vascular injury. Specific leukocyte subsets, including IL-17-producing T helper type 17 (TH17) cells, drive inflammation and contribute to renal immunopathology. B-cell- activating factor (BAFF) might increase the generation of new autoreactive B cells, inhibit B cell apoptosis and stimulate the differentiation of B cells into immunoglobulin-producing plasma cells. Infiltrating leukocytes might also provide a source of nuclear antigens and cytokines, such as interferon (IFN) α, tumour necrosis factor (TNF), IL-1 and IL-6. High mobility group box 1 (HMGB1), biglycan and histones released from immune cells can bind Toll-like receptors (TLRs) expressed by endothelial cells, leading to an inflammatory response. Inaddition, anti-double-stranded DNA (anti-dsDNA) antibodies can induce fibronectin secretion in proximal renal tubular epithelial cells, leading to TGFβ activation and collagen synthesis. Activation of the apoptosis regulator BCL-2 might also contribute to the development of tubulointerstital inflammation, whereas antiphospholipid antibody-induced thrombosis might contribute to the development of interstitial vascular inflammation. GBM, glomerular basement membrane; TCR, T-cell receptor; Treg, regulatory T cell.
Yu, F. et al. (2017) Redefining lupus nephritis: clinical implications of pathophysiologic subtypes
Nat. Rev. Nephrol. doi: /nrneph