Anti-C1q autoantibodies amplify pathogenic complement activation in systemic lupus erythematosus.
Patients with systemic lupus erythematosus (SLE) often develop glomerulonephritis (i.e., inflammation in the glomeruli of the kidney), commonly referred to as lupus nephritis. Patients with lupus nephritis typically have autoantibodies to the complement classical pathway protein C1q. Whether these anti-C1q antibodies play any role in the development of lupus nephritis has been unclear. In this issue of the JCI, a new study demonstrates that anti-C1q antibodies can amplify glomerular injury but only when they are bound within the glomerulus to C1q that has been already brought to that site by other types of glomerular-reactive autoantibodies. These studies are the first, to our knowledge, to provide a causal link between anti-C1q antibodies and target organ damage in SLE.
Holers
V Michael
VM
Departments of Medicine and Immunology, University of Colorado Health Sciences Center, Denver, Colorado, USA. michael.holers@uchsc.edu
D000818:Animals; D001323:Autoantibodies / Q000276:immunology* / Q000378:metabolism; D003167:Complement Activation / Q000276:immunology* / Q000502:physiology; D015922:Complement C1q / Q000276:immunology* / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D051379:Mice
D001323:Autoantibodies; D015922:Complement C1q