| First Author | Biancone L | Year | 1995 |
| Journal | Kidney Int | Volume | 48 |
| Issue | 2 | Pages | 458-68 |
| PubMed ID | 7564113 | Mgi Jnum | J:30194 |
| Mgi Id | MGI:77708 | Doi | 10.1038/ki.1995.314 |
| Citation | Biancone L, et al. (1995) Inhibition of the CD40-CD40ligand pathway prevents murine membranous glomerulonephritis. Kidney Int 48(2):458-68 |
| abstractText | Several forms of glomerulonephritis are induced by antibodies against self or foreign antigens. Normal B lymphocyte antibody production requires T cell costimulatory signals provided in part by T cell surface expression of gp39/CD40ligand (CD40L) that engages the B cell receptor CD40 and induces B cell differentiation and immunoglobulin class switching. We assessed the effect of disrupting the CD40L-CD40 costimulatory pathway, using a CD40-Ig fusion protein, on the development of membranous glomerulonephritis (MGN) in the mouse. MGN is induced by mouse antibodies that recognize and bind to exogenously administered rabbit anti-mouse renal tubular brush border (RbAMBB) IgG immobilized in the glomerular capillary wall. MGN did not occur in nude mice, showing the need of the T cell function. C57Bl/10 mice immunized with RbAMBB and treated with CD40-Ig fusion protein displayed a delayed autologous response and absence of MGN lesions, while control fusion proteins failed to prevent the development of the disease. These observations provide evidence that disruption of the CD40-CD40L costimulatory pathway can prevent the development of MGN by suppressing T cell-dependent antibody production. |
