IgA nephropathy: immune mechanisms beyond IgA mesangial deposition.
IgA nephropathy is attributable to mesangial IgA immune complex deposition. The pathogenic potential of frequently colocalized IgG deposits may depend on polarized T-helper cytokines that modulate Fcgamma receptors of infiltrating macrophages, leading to either activation or inhibition that determines glomerular injury.
Rifai
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Department of Pathology and Laboratory Medicine, Lifespan Academic Medical Center, Brown University School of Medicine, Providence, Rhode Island, USA. Arifai@Lifespan.org
D000818:Animals; D000936:Antigen-Antibody Complex / Q000378:metabolism; D004195:Disease Models, Animal; D005922:Glomerulonephritis, IGA / Q000209:etiology* / Q000276:immunology* / Q000503:physiopathology; D007070:Immunoglobulin A / Q000378:metabolism*; D007074:Immunoglobulin G / Q000378:metabolism; D008264:Macrophages / Q000473:pathology / Q000502:physiology; D050527:Mesangial Cells / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D017452:Receptors, IgG / Q000502:physiology
D000936:Antigen-Antibody Complex; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D017452:Receptors, IgG