Critical role of complement in antibody mediated rejection in kidney transplantation

Figure 1 Complement activation pathways. Ag-Ab: Antigen-antibody; C1inh: C1 esterase inhibitor; MASP-1: Mannan-binding lectin-associated serine protease-1; MASP-2: Mannan-binding lectin-associated serine protease-2; MCP: Membrane cofactor protein; DAF: Decay accelerating factor.

Figure 2 The role of the classical complement pathway in acute antibody-mediated rejection in kidney transplant recipients. HLA class: Human leucocyte antigen class; DSA: Donor specific antibody; PTC: Peritubular capillaritis; NK cells: Natural killer cells; APC: Antigen presenting cell; TCR: T cell receptor.

Figure 3 The role of complement in the pathogenesis of ischemic reperfusion injury in renal transplantation. MASP-1: Mannan-binding lectin-associated serine protease-1; MASP-2: Mannan-binding lectin-associated serine protease-2; MAC: Membrane attack complex; ROS: Reactive oxygen species; NADPH oxidase: Nicotinamide adenine dinucleotide phosphate oxidase; DAMP: Damage-associated molecular patterns; PAMP: Pathogen-associated molecular patterns.

Figure 4 Histopathology of acute antibody-mediated rejection. A: Acute glomerulitis. Some of the glomerular capillary lumens are obliterated by inflammatory cell infiltration and/or endothelial cell swelling (arrow). [hematoxylin and eosin (HE), × 400]; B: Foci of mild peritubular capillaritis with up to 4 inflammatory cells in capillary lumens (ptc1) (arrows) (HE, × 400); C: An interlobar sized artery showing transmural arteritis (v3) (HE, × 400); D: Diffuse C4d positivity (C4d) (C4d3) in peritubular capillaries. Glomerular mesangial positivity serves as the internal control (Flourescein isothiocyanate, immunofluorescence for C4d, × 200).