Open AccessAn acute model for IgA‐mediated glomerular inflammation in rats induced by monoclonal polymeric rat IgA antibodies
Author(s) -
STAD R. K.,
BRUIJN J. A.,
GIJLSWIJKJANSSEN D. J.,
ES L.A.,
DAHA M. R.
Publication year - 1993
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1993.tb03430.x
Subject(s) - glomerular mesangium , immunoglobulin a , nephritis , glomerulonephritis , mesangium , proteinuria , inflammation , immunoglobulin e , antibody , immunology , endocrinology , antigen , chemistry , medicine , immunoglobulin g , kidney
SUMMARY An acute model Tor IgA‐mediated glomerular inflammation in rats was induced by the in situ deposition of IgA directly into the glomerular mesangium. F(ab') 2 anti‐Thyl MoAb was used to anchor an antigen. DNP (2,4‐dinitrophenol), in the glomeruli of rats. Subsequent infusion of rat polymeric (p‐) or monomeric (m‐) IgA MoAb with specificity for DNP resulted in mesangial deposition of IgA in both groups of rats. However, acute proteinuria was observed only in p‐IgA‐treated rats and not in PBS‐ or m‐IgA‐treated rats. Immunofluorescence analysis revealed deposition of C3 in an identical pattern to that of IgA in the glomeruli of p‐IgA‐treated rats. No mesangial deposits of C4 or Clq were seen in these animals. Rats receiving m‐IgA or PBS displayed no detectable C3, C4 or Clq deposition. The amount of proteinuria in p‐IgA‐treated rats was related to the amount of deposited C3. The presence of intraglomerular monocytes was only observed 2 days after p‐IgA injection. By light microscopy, aneurysm formation, mesangial hypercellularity and matrix expansion were seen only in p‐IgA‐treated rats. However, by 37 days post‐injection complete resolution of the lesions was observed. No histological renal changes were observed in PBS‐ or m‐IgA‐trcatcd rats. In conclusion, an acute form of IgA‐mediated nephritis in rats was induced by p‐lgA but not by m‐IgA. This reproducible model provides a basis for further study into the mechanisms of IgA‐mediated glomerular inflammation.