Literature DB >> 606450

A study of the material inhibiting EAC-rosette formation in the sera of patients with nephropathies.

M D Smith, P J Verroust, C Adam, M Galceran, L Morel-Maroger.   

Abstract

Significant levels of EAC-rosette inhibition compared to control subjects were found in the sera of patients with focal and segmental hyalinosis (FSH), membranoproliferative glomerulonephritis (MPGN) and extra-membranous glomerulonephritis (EGN). In patients with IgA disease, although some sera produced high levels of inhibition, the group as a whole did not differ significantly from the controls. Evidence was obtained suggesting that the rosette inhibitory activity was due to immune complexes (IC) bearing C3 rather than C3 fragments. Firstly, the inhibitory activity was precipitable by 4% PEG, a concentration which does not precipitate the C3 fragments. Secondly, the inhibitory activity was selectively removed from the PEG precipitates by an anti-human immunoglobulin G immunoabsorbent. Finally, since it had been suggested that in some instances an unknown serum factor could inhibit EAC-rosette formation and activation of the alternative pathway of complement, the latter was studied and found to be normal in all the sera studied. Taken together, these results suggest that the inhibition of EAC-rosette formation obtained with the sera of the patients studied was due to the presence in these sera of some material behaving as IC. No clear-cut association was, however, seen between rosette inhibition and the presence or absence of Ig or C3 deposits in the kidney.

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Year:  1977        PMID: 606450      PMCID: PMC1541153     

Source DB:  PubMed          Journal:  Clin Exp Immunol        ISSN: 0009-9104            Impact factor:   4.330


  14 in total

1.  ANTIGEN-ANTIBODY CROSSED ELECTROPHORESIS.

Authors:  C B LAURELL
Journal:  Anal Biochem       Date:  1965-02       Impact factor: 3.365

2.  Mechanism of binding of soluble immune complexes to lymphocytes.

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Journal:  Cell Immunol       Date:  1973-06       Impact factor: 4.868

3.  Inhibition of complement-dependent lymphocyte rosette formation: a possible test for activated complement products.

Authors:  G Ezer; A R Hayward
Journal:  Eur J Immunol       Date:  1974-02       Impact factor: 5.532

4.  Inhibition of C3 conversion after allotransplantation.

Authors:  R E Spitzer; A E Stitzel
Journal:  Transplantation       Date:  1972-02       Impact factor: 4.939

5.  Complement as a regulator of interactions between immune complexes and cell membranes.

Authors:  G W Miller; V Nussenzweig
Journal:  J Immunol       Date:  1974-08       Impact factor: 5.422

6.  Haemolytic diffusion plate assays for factors B and D of the alternative pathway of complement activation.

Authors:  A Martin; P J Lachmann; L Halbwachs; M J Hobart
Journal:  Immunochemistry       Date:  1976-04

7.  Inhibition of the alternative pathway of complement activation by a serum factor generated during transplant rejection.

Authors:  R Spitzer; A Stitzel; L Florio; J Urmson
Journal:  Immunochemistry       Date:  1976-05

8.  Autoimmune New Zealand mouse. Alterations in C3 receptors, complement-induced clumps and follicular adherence of immune complexes.

Authors:  A Arnaiz-Villena; P Sheldon
Journal:  Immunology       Date:  1975-12       Impact factor: 7.397

9.  Complement-dependent release of immune complexes from the lymphocyte membrane.

Authors:  G W Miller; P H Saluk; V Nussenzweig
Journal:  J Exp Med       Date:  1973-09-01       Impact factor: 14.307

10.  Pathogenesis of chronic disease associated with persistent lymphocytic choriomeningitis viral infection. I. Relationship of antibody production to disease in neonatally infected mice.

Authors:  M B Oldstone; F J Dixon
Journal:  J Exp Med       Date:  1969-03-01       Impact factor: 14.307

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  1 in total

1.  Analysis of circulating IgA and detection of immune complexes in primary IgA nephropathy.

Authors:  P Lesavre; M Digeon; J F Bach
Journal:  Clin Exp Immunol       Date:  1982-04       Impact factor: 4.330

  1 in total

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