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KMID : 0357319950300040451
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Journal of the Korean Society for Microbiology
1995 Volume.30 No. 4 p.451 ~ p.462
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Role of Antigens in Experimental IgA Nephropathy in Mouse'
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Abstract
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IgA nephropathy (Berger's disease) is the most common form of primary glomerulonephritis worldwide and defined by the dominant or codominant deposition of IgA in the mesangium. IgA immune complexes are believed to be of critical pathogenetic
importance
in this disease. However, the mechanisms through which the IgA immune complexes induce glomerular damage areunknown. Complement activation is thought to play an important role in the pathogenesis but several studies failed to find a correlation
between
complement activation and the severity of IgA nephropathy. Also it has been demonstrated that IgA aggregates do not activate the complement system. Based on the hypothesis that the antigen in immune complexes is a critical factor to glomerular
damage,
we tried to make up a passive experimental model of IgA nephropathy in mice by administration of dinitrophenylated albumin (DNP-Albumin) and Ficoll (DNP-Ficoll) as an antigen and IgA obtained from MOPC 315 cell line as an antibody. Mice that
received
only IgA-anti-DNP developed insignificant glomerular Iga and C, deposits. In contrast, mice treated with antigen and antibody developed significant histopathologic changes and mesangial deposition of IgA. C3 and fibrinogen. It was concluded that
the
antigen in immune complexes plays a critical role in glomerular damage in IgA nephropathy.
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KEYWORD
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