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RI
Surface Densities and Mediator Release by Anti-IgE-Infusions Is Reversible In Vitro and In Vivo1
*
Department of Medicine, Division of Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore MD 21224; and
Genentech, South San Francisco, CA 94080
Previously, infusions of an anti-IgE mAb (rhumAb-E25) in
subjects decreased serum IgE levels, basophil IgE and Fc
RI
surface density, and polyclonal anti-IgE and Ag-induced basophil
histamine release responses. We hypothesized that these effects would
be reversed in vivo by discontinuation of infusions and in vitro by
exposing basophils to IgE. Subjects received rhumAb-E25 biweekly for 46
wk. Blood samples taken 0–52 wk after rhumAb-E25 were analyzed for
serum IgE and basophil expression of IgE, FcRI, and CD32.
Basophil numbers were unaffected by infusions. Eight weeks after
infusions, free IgE levels rose in vivo but did not reach baseline.
Basophil IgE and FcRI rose in parallel with free IgE while CD32
was stable. FcRI densities, measured by acid elution, returned to
80% of baseline, whereas histamine release responses returned to
baseline. Basophils cultured with or without IgE or IgG were analyzed
for expression of IgE, FcRI, and CD32. By 7 days with IgE,
expression of IgE and FcRI rose significantly, whereas cultures
without IgE declined. IgE culture did not effect CD32. IgG culture did
not effect expression of any marker. The present results strongly
suggest that free IgE levels regulate FcRI expression on
basophils.
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