Three pathogenic determinants in immune nephritis--anti-glomerular antibody specificity, innate triggers and host genetics.
The prevailing notion is that lupus nephritis is mediated by autoantibodies, particularly those that bind to DNA and/or glomeruli. However it has become apparent that the development of immune-mediated renal disease is contingent upon additional factors including innate stimuli and host genetics. The purpose of this review is to evaluate our current understanding of three factors that can potentially influence immune-mediated renal disease: (1) Anti-glomerular/DNA antibodies (Abs), (2) Innate triggers, including Toll-Like Receptor (TLR) stimulation, and (3) the genetic makeup of the host.
Wu
Tianfu
T
Department of Internal Medicine (Rheumatology) and the Center for Immunology, University of Texas Southwestern Medical School, Dallas, TX 75235, USA.
Mohan
Chandra
C
D000818:Animals; D000974:Antibodies, Antinuclear / Q000276:immunology; D000918:Antibody Specificity; D001323:Autoantibodies / Q000276:immunology*; D004247:DNA / Q000276:immunology; D007113:Immunity, Innate; D007678:Kidney Glomerulus / Q000276:immunology*; D008181:Lupus Nephritis / Q000235:genetics* / Q000276:immunology*; D051379:Mice; D051193:Toll-Like Receptors / Q000378:metabolism
D000974:Antibodies, Antinuclear; D001323:Autoantibodies; D051193:Toll-Like Receptors; D004247:DNA