Abstract
Ankylosing spondylitis and IgA nephropathy share some immunologic features, eg, elevated serum IgA and IgA-immune complex levels. These entities are frequently found as being associated. IgA and IgA immune complex catabolism involves asialoglycoprotein receptors and specific IgA Fc receptors (FcalphaR or CD89) on tissue and blood cells. Recent studies revealed impaired CD89 expression in both diseases. These abnormalities, which are associated with receptor saturation, might generate the increase in serum IgA and IgA immune complex levels by either altered recycling or failure of degradation. This article reviews the literature on IgA abnormalities and discusses the potential role of FcalphaR in IgA nephropathy and AS and the consequences of its similar defect in the two diseases.
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