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Responsiveness for Mouse IgG 2b Antibodies to the Human α/β T‐Cell Receptor/CD3 Complex: Evidence for Genetic Determination and Low Grade Antibody Cross‐Linking Not Mediated by Known Feγ Receptors
Author(s) -
SCHLITT H. J.,
SCHWINZER R.,
WONIGEIT K.
Publication year - 1993
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1993.tb02561.x
Subject(s) - antibody , receptor , biology , peripheral blood mononuclear cell , immunology , stimulation , t cell receptor , microbiology and biotechnology , cd3 , antigen , t cell , immune system , cd8 , endocrinology , genetics , in vitro
Mouse IgG 2a and IgG 3 antibodies directed to the human T‐cell receptor/CD3 complex stimulate peripheral blood mononuclear cells in almost all individuals. By contrast, responder and non‐responder individuals exist for the stimulatory effect of mouse IgG 1 and IgG 2b antibodies. Whereas responsiveness to IgG 1 antibodies is rather frequent (60–70%) and is known to be determined by an FcγRII polymorphism on the accessory cells, little is known about the underlying factors of the rare (6%) IgG 2b responsiveness. In this study it is shown that (1) IgG 2b responsiveness is genetically determined with a dominant pattern of inheritance; (2) IgG 2b responsiveness is determined by a radioresistant feature of responder accessory cells which can be substituted by artificial cross‐linking, but not by IL‐1β or IL‐2; (3) stimulation of peripheral blood mononuclear cells of an IgG 2b responder by IgG 2b antibodies requires rather high antibody concentration compared with stimulation by IgG 2a antibodies; (4) the stimulation leads to proliferation and IL‐2 receptor expression, but no measurable IL‐2 production; (5) antibody binding to known Fey receptors (FcγRI, FcγRII, FcγRIIT) is not involved in the stimulatory effect of the IgG 2b antibodies in responders. These results demonstrate that responsiveness to IgG 2b antibodies against the TcR/CD3 complex depends on a genetically determined feature of accessory cells that is not identical with any of the known Fcγ receptors. Most likely, the stimulatory effect observed in IgG 2b responders is explained by a low grade cross‐Unking of the antibody by a not yet identified polymorphic structure on the surface of accessory cells.