Complement-fixing IgG1 constitutes a new subclass of mouse IgG View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1979-10

AUTHORS

Peter L. Ey, Stephen J. Prowse, Charles R. Jenkin

ABSTRACT

Four IgG isotypes (IgG1, IgG2a, IgG2b, IgG3) have been distinguished in the mouse1–3. The similarity of the physico-chemical properties of the different isotypes has to a large extent prevented their purification from serum and this has complicated functional studies on IgG antibodies in sera from infected or immunised mice1,2,4. The availability of immunoglobulin-secreting plasmacytomas5, however, has made the production of isotype-specific antisera possible; the use of these antisera has shown immunoglobulin of each isotype to exist in sera from normal animals3,5,6. IgG1 antibodies, partially separated from IgG2 by electrophoresis in agar, have been reported2 to be incapable of sensitising sheep red blood cells (SRBC), passively coated with antigen, for lysis by complement (C) although the antibodies agglutinated the cells and also mediated passive cutaneous anaphylactic (PCA) reactions in the mouse. The IgG2 antibodies, which mediated PCA reactions in the guinea pig but not in the mouse, lysed the antigen-coated SRBC in the presence of mouse C. It seems on the basis of this single report that mouse IgG1 has been widely accepted6–8 to be a ‘non-C-fixing’ class of immunoglobulin—one which, on association with antigen, is unable to activate C. We have now purified IgG1 from the serum of mice immunised with SRBC and in this report present evidence that the IgG1 antibodies are not only haemolytic in the presence of C, but that they apparently account for more than half of the SRBC-specific, C-fixing IgG antibodies in the serum of the immunised animals. More... »

PAGES

492-493

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/281492a0

DOI

http://dx.doi.org/10.1038/281492a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1044992084

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/114859


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