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The effectiveness of different rat IgG subclasses as IgE‐blocking antibodies in the rat basophil leukaemia cell model
Author(s) -
Philips J R,
Brouwer W,
Edwards M,
Mahler S,
Ruhno J,
Collins A M
Publication year - 1999
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1046/j.1440-1711.1999.00801.x
Subject(s) - degranulation , immunoglobulin e , antibody , antigen , blocking antibody , immune system , receptor , basophil , chemistry , monoclonal antibody , microbiology and biotechnology , fc receptor , immunology , biology , biochemistry
The degranulation of mast cells in an allergic response is initiated by the aggregation of high‐ affinity IgE receptors (FcεRI) by IgE and antigen. Recently it has been shown that such degranulation can be inhibited by cross‐linking FcεRI and low‐affinity IgG receptors (FcγRII) which are also expressed by mast cells. The ability of various monoclonal antibodies to block the degranulation of rat basophil leukaemia (RBL) cells sensitized with IgE antidinitrophenyl (DNP) antibodies has been investigated. Sensitized cells were challenged with immune complexes formed using varying concentrations of antigen, and of both high‐ and low‐valency antigen. It is reported here that rat IgG1 antibodies, which are associated in the rat with a Th1‐type response, act as highly effective blocking antibodies over a wide concentration range. Rat IgG2a antibodies, which are associated with a Th2‐type response, were able only to inhibit degranulation when immune complexes were formed with very low concentrations of high‐valency antigen (DNP 32 ‐HSA). Under these conditions, some inhibitory activity was seen with high‐affinity murine IgA anti‐DNP but not with low‐affinity rat IgG2b anti‐DNP antibody‐containing immune complexes. In addition to this inhibitory activity, IgG2a antibodies were shown to be capable of inducing degranulation of cells via unoccupied FcεRI. These results demonstrate that blocking activity may arise via both inhibitory receptors and by masking of antigen.