Factor friction: protective and pathogenic roles for complement factors in immune complex glomerulonephritis.
The classical pathway of complement is activated in patients with immune complex glomerulonephritis. However, Alexander et al. demonstrate that factor H, an alternative pathway regulator, is critical for protecting mice from immune-complex-mediated glomerular injury. In mice that lack factor H, signaling through the C5a receptor is necessary for the development of injury. These results suggest that factor H may be critical for limiting injury in a wide range of autoimmune and inflammatory renal diseases.
Division of Nephrology, University of Colorado Denver School of Medicine, Aurora, Colorado 80045, USA. Joshua.Thurman@ucdenver.edu
Joshua M
JM
Thurman
D000818:Animals; D017242:Complement Factor H / Q000172:deficiency / Q000276:immunology; D005921:Glomerulonephritis / Q000276:immunology*; D000081208:Hereditary Complement Deficiency Diseases; D007105:Immune Complex Diseases / Q000276:immunology*; D007674:Kidney Diseases / Q000276:immunology*; D008297:Male; D044087:Receptor, Anaphylatoxin C5a / Q000235:genetics* / Q000276:immunology*; D015432:Glomerulonephritis, Membranoproliferative
D044087:Receptor, Anaphylatoxin C5a; D017242:Complement Factor H