1. Figure 3 Biologics that attenuate effector responses in the kidney
Figure 3 | Biologics that attenuate effector responses in the kidney. Autoantigen recognition in the kidney by autoimmune CD4+ T cells and autoantibodies results in recruitment and activation of innate effector leukocytes (mainly neutrophils and macrophages). These leukocytes induce pathological inflammation by releasing molecular mediators, predominantly inflammatory cytokines (IL-Iβ, IL-6 and TNF), all of which can be targeted by biologics. Leukocyte accumulation is facilitated by endothelial adhesion molecules, some of which (VLA-4 and LFA-1) can be targeted by biologics. Autoantibodies activate complement to generate the potent pro-inflammatory anaphylotoxin C5a and the terminal attack complex C5b–C9 to induce sub-lytic cell damage. Eculizumab limits complement activation and soluble FcγRllb can inactivate immune complexes. Biologics are highlighted in purple.
Holdsworth, S. R. et al. (2016) Biologics for the treatment of autoimmune renal diseases
Nat. Rev. Nephrol. doi: /nrneph