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Neuropeptide‐mediated regulation of hapten‐specific IgE responses in mice I. Substance P‐mediated isotype‐specific suppression of BPO‐specific IgE antibody‐forming cell responses induced in vivo and in vitro
Author(s) -
Carucci John A.,
Auci Dominick L.,
Herrick Christina A.,
Durkin Helen G.
Publication year - 1995
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.57.1.110
Subject(s) - immunoglobulin e , biology , isotype , immunology , in vivo , neurotensin , vasoactive intestinal peptide , hapten , neuropeptide , keyhole limpet hemocyanin , in vitro , antibody , hemocyanin , endocrinology , medicine , receptor , monoclonal antibody , biochemistry , microbiology and biotechnology
The ability of substance P (SP) to regulate peak benzyl‐penicilloyl (BPO)‐specific IgE antibody‐forming cell (AFC) responses in vivo and the ability of SP and other neuropeptides to regulate BPO‐specific memory IgE AFC responses induced in vitro was determined. SP injected subcutaneously into BPO‐keyhole limpet hemocyanin (BPO‐KLH)‐sensitized mice at the time of peak IgE responses suppressed these responses within 48 h (>90%). The suppression obtained was IgE isotype‐specific, dose‐dependent, and transient. When spleen cells from immunized mice were cultured for 5 days with BPO‐KLH, peak memory IgE AFC responses were induced in vitro. Inclusion of either SP or vasoactive intestinal peptide (VIP), but not neurotensin, serotonin, somatostatin, or gastrin, in cultures suppressed these responses in isotype‐specific, dose‐dependent fashion (70%). SP‐, but not VIP‐mediated suppression of IgE responses was abrogated by inclusion of anti‐IFNγ in culture. J. Leukoc. Biol. 57: 110–115; 1995.