Literature DB >> 3958495

Only the initial binding of cationic immune complexes to glomerular anionic sites is mediated by charge-charge interactions.

V J Gauthier, M Mannik.   

Abstract

The role of charge-charge interactions between cationic immune complexes and the anionic sites on the glomerular basement membrane was examined. For this purpose, soluble immune complexes at fivefold antigen excess were prepared with human serum albumin and cationized rabbit antibodies to this protein. When unrelated cationic proteins, protamine sulfate or cationized rabbit serum albumin, were given 1 min before the cationized immune complexes, glomerular immune deposits did not form. Cationic immune complexes allowed to deposit in glomeruli could readily be displaced by protamine sulfate or cationized rabbit serum albumin injected 1 min after the immune complexes. If the same cationic molecules were injected 1 hr after the immune complexes, the complexes could not be displaced from glomeruli. In contrast, cationic complexes that were deposited in glomeruli in the presence of a very high degree of antigen excess in circulation to prevent their condensation into larger complexes in glomeruli were readily displaced at 1 min and 1 hr with protamine sulfate or with cationized rabbit serum albumin. On the basis of these results, we concluded that the initial binding of cationic immune complexes to glomeruli occurs by charge-charge interactions. Once the immune complexes in glomeruli condense to larger deposits, forces other than charge-charge interactions are responsible for their retention in glomeruli.

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Year:  1986        PMID: 3958495

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  6 in total

1.  Antigenic charge as a factor in resistance to immunosuppressive therapy.

Authors:  S G Adler; H Y Wang; A H Cohen; W A Border
Journal:  Am J Pathol       Date:  1988-06       Impact factor: 4.307

Review 2.  Mechanisms of immune deposit formation in renal glomeruli.

Authors:  M H Wener; M Mannik
Journal:  Springer Semin Immunopathol       Date:  1986

3.  Specific increases in urinary excretion of anti-DNA antibodies in lupus mice induced by lysozyme administration: further evidence for DNA-anti-DNA immune complexes in the pathogenesis of nephritis.

Authors:  T Yamamoto; M Nagase; A Hishida; N Honda
Journal:  Clin Exp Immunol       Date:  1993-01       Impact factor: 4.330

4.  Mechanism of formation of subepithelial electron-dense deposits in active in situ immune complex glomerulonephritis.

Authors:  S Kagami; K Kawakami; K Okada; Y Kuroda; T Morioka; F Shimizu; T Oite
Journal:  Am J Pathol       Date:  1990-03       Impact factor: 4.307

5.  IgG3 deficiency extends lifespan and attenuates progression of glomerulonephritis in MRL/lpr mice.

Authors:  Neil S Greenspan; Myro A Lu; Jacob W Shipley; Xuedong Ding; Qing Li; Dilara Sultana; Maria Kollaros; John R Schreiber; Pingfu Fu; Chaim Putterman; Steven N Emancipator
Journal:  Biol Direct       Date:  2012-01-16       Impact factor: 4.540

6.  Anti-DNA autoantibodies initiate experimental lupus nephritis by binding directly to the glomerular basement membrane in mice.

Authors:  Meera R Krishnan; Congmiao Wang; Tony N Marion
Journal:  Kidney Int       Date:  2012-02-01       Impact factor: 10.612

  6 in total

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