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Intercellular adhesion molecule (ICAM‐1) inhibition can induce tolerance in vivo
Author(s) -
CHARLTON B.,
GUYMER R. H.,
SLATTERY R. M.,
MANDEL T. E.
Publication year - 1991
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 - 10.1038/icb.1991.14
Subject(s) - antigen , in vivo , immunology , major histocompatibility complex , antibody , intercellular adhesion molecule 1 , intercellular adhesion molecule , intracellular , chemistry , biology , microbiology and biotechnology , cell adhesion molecule , cell , cell adhesion , biochemistry
Summary Antigen specific unresponsiveness can be induced in vivo by administration of antibody against CD4, major histocompatibility complex (MHC) Class II or LFA‐I at the time of antigen exposure. Since target cell depletion is not necessary for this effect it was hypothesized that interference with intercellular interaction was responsible. To test this hypothesis, antibody against the ligand for LFA‐1, ICAM‐l, was administered during primary immunization with human γ‐globulin (HGG) and long‐term secondary antibody responses monitored. It was found that HGG specific unresponsiveness resulted from this treatment (<10% of normal secondary antibody response), Delayed‐type hypersensitivity responses to HGG were also suppressed suggesting unresponsiveness in some T cell subsets. These findings suggest a role for ICAM‐I/LFA‐1 interaction in determining the long‐term outcome of contact with antigen.