Immune complex formation in IgA nephropathy: CD89 a 'saint' or a 'sinner'?
New data suggest that a soluble form of the IgA receptor CD89 may be protective against development of progressive renal injury in IgA nephropathy (IgAN). Understanding how IgA triggers shedding of CD89 from myeloid cell surfaces could help clarify the process of immune complex formation in IgAN, and measurement of this soluble form of CD89 may in the future prove a useful prognostic indicator of end-stage renal disease in this common glomerulonephritis.
John Walls Renal Unit, Leicester General Hospital, Leicester, UK. Jb81@le.ac.uk
Joanna K
JK
Boyd
Jonathan
J
Barratt
D000936:Antigen-Antibody Complex / Q000378:metabolism*; D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D018450:Disease Progression; D005922:Glomerulonephritis, IGA / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007070:Immunoglobulin A / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000175:diagnosis / Q000453:epidemiology / Q000378:metabolism; D020641:Polymorphism, Single Nucleotide / Q000235:genetics; D011379:Prognosis; D011961:Receptors, Fc / Q000235:genetics / Q000378:metabolism*; D012307:Risk Factors
D000936:Antigen-Antibody Complex; D015703:Antigens, CD; D015415:Biomarkers; C036832:Fc(alpha) receptor; D007070:Immunoglobulin A; D011961:Receptors, Fc