Goodpasture's epitope in development of experimental autoimmune glomerulonephritis in rats.
Goodpasture's epitope in development of experimental autoimmune glomerulonephritis in rats.
复制标题
古德帕斯彻表位在大鼠实验性自身免疫性肾小球肾炎发展中的作用。
DOI：
10.1038/ki.1996.49
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发表时间：
1996
影响因子：
19.6
通讯作者：
Fox,J
中科院分区：
文献类型：
--
作者：
Bolton,WK;Luo,AM;Fox,P;May,W;Fox,J
Goodpasture's epitope in development of experimental autoimmune glomerulonephritis in rats.The Goodpasture's epitope (GP) has recently been localized to the last 36 AA of the non-collagenous (NC1) domain of theα3chain of type IV collagen [α3(IV)]. Sinceα3(IV) induces glomerulonephritis (GN) in rats and rabbits, the purpose of the present study was to determine if the GP epitope itself could induce GN. We immunized rats with synthetic peptides of GP epitope, 36-mer, alone or as protein conjugates. Rats immunized with bovine GBM served as positive controls. Peptide immunized rats developed high titer antibodies to peptides, but only unconjugated 36-mer induced antibody against human and bovine GBM, but not to rat GBM. Acidic residues and the full length 36-mer were important in production of GBM reactive antibodies. Positive controls developed antibody to GBM without reactivity against 36-mer, had IgG and fibrin on the basement membrane, GN and proteinuria. Kidney eluted antibody was reactive with rat, bovine, and human GBM but not 36-mer. GN rat lymphocytes underwent blast transformation to GBM but not peptide, and peptide immunized animals responded only to the respective peptides. None of the animals immunized with GP peptide epitope, despite the development of anti-peptide antibodies or anti-GBM antibodies, developed anyin vivofixation of antibody to the GBM, abnormal proteinuria, or GN. The present study shows that the GP epitope is sufficient to induce an immune response to the epitope, but it is not sufficient to induce GN. This demonstrates that other factors or epitopes are important in the pathogenicity of GBM induced GN in this model. These remain to be delineated.
