1. Figure 1 Sequence of events in the development of autoimmune nephritis
Figure 1 | Sequence of events in the development of autoimmune nephritis. Immune complexes and activated complement components accumulate at the glomerular basement membrane and initiate barrier disruption, permitting the passage of low molecular weight molecules containing damage-associated molecular patterns (DAMPs), which are recognized by innate immune cells, including dendritic cells (DCs), innate lymphoid cells (ILCs) and kidney cells. These cells recruit and activate T cells, including δγT cells, double-negative (DN) T cells, and T-helper (TH) type 17 cells, by releasing cytokines such as IL-23, leading to the release of IL-17 and the recruitment of neutrophils and natural killer (NK) cells. T follicular helper (TFH) cells and TH17 cells promote the production of antibodies by B cells. Production of IFNγ by cytotoxic T lymphocytes (CTL), TH1 cells, NK cells and TH17 cells stimulates the recruitment of macrophages. T cells therefore orchestrate the autoimmune response and, together with neutrophils and macrophages, amplify and sustain inflammation through the further release of cytokines and chemokines, the recruitment, activation and proliferation of B cells, and also by stimulating intrinsic kidney cells to cause aberrant function and irreversible kidney damage. IFNγ, interferon γ; TLR, Toll-like receptor.
Suárez-Fueyo, A. et al. (2017) T cells and autoimmune kidney disease
Nat. Rev. Nephrol. doi: /nrneph