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Induction of H‐2‐specific antibodies by injections of syngeneic Sendai virus‐coated cells
Author(s) -
Kievits Femia,
Rocca Anna,
Opolski Adam,
Limpens Jacqueline,
Leupers Tine,
Kloosterman Tinie,
Boerenkamp Walter J.,
Pla Marika,
Ivanyi Pavol
Publication year - 1987
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830170106
Subject(s) - sendai virus , antibody , cytotoxic t cell , biology , virology , microbiology and biotechnology , antigen , virus , spleen , immunology , in vitro , biochemistry
Abstract The capacity of the B cell immunoglobulin receptor to recognize complexes of Sendai viral and H‐2 b antigens was investigated by studying the antibody response to injections of syngeneic Sendai virus‐coated (SV + ) spleen cells in C57BL/6 (B6) mice. Almost all mice produced alloreactive anti‐H‐2 lymphocytotoxic antibodies. In contrast, such antibodies were found very exceptionally in mice injected with normal (SV − ) cells or with Sendai virus (SV) only. The reaction pattern of the cytotoxic antibodies induced was variable and ranged from almost anti‐private to widely cross‐reactive serotypes. The results of reactions on H‐2‐congenic, ‐recombinant and ‐mutant mouse strains, and of capping and immunoprecipitation experiments showed that the cytotoxic antibodies were directed against H‐2 class I molecules. The anti‐H‐2 antibodies exhibited enhanced binding for SV + target cells, but absorption experiments showed that this was not the result of cross‐reactions with cell surface Sendai viral determinants or with a molecular complex of H‐2 plus SV. This conclusion was supported by the observation that syngeneic SV + cells were not the predominant targets for the induced lymphocytotoxic antibodies. Our results do not support the existence of MHC‐restricted antiviral antibodies, but show the induction of anti‐class I H‐2 alloantibodies by injections with syngeneic SV‐coated cells. We present a model for regular induction of anti‐H‐2 antibodies without intentional alloimmunization.