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Departments of
*
Cell Biology, Neurobiology, and Anatomy and
Microbiology and Immunology, Loyola University Medical Center, Maywood, IL 60153
The mechanism by which the Th2 cell-dependent Ab response is
modulated by the sympathetic neurotransmitter norepinephrine (NE) was
investigated. Our model system used the severe combined immunodeficient
(scid) mouse that was depleted of NE with
6-hydroxydopamine before reconstitution with a clone of
ß2-adrenergic receptor (ß2AR)neg
KLH-specific Th2 cells and resting trinitrophenyl (TNP)-specific
ß2ARpos B cells enriched from the spleens of unimmunized
mice. Following challenge with TNP-keyhole limpet hemocyanin (KLH), Ab
production in these mice was hapten-, carrier-, and allotype-specific
as well as MHC restricted. Depletion of NE resulted in a 50–75%
suppression of the primary anti-TNP IgM response compared with that
of NE-intact controls, while the secondary IgM response returned to
control levels. In contrast, both the primary and secondary
anti-TNP IgG1 responses were suppressed by 85 and 40%,
respectively. Using NE-intact mice exposed to either a ßAR- or
AR-selective antagonist, the effect of NE on the Ab response was
shown to be mediated by the ßAR. In addition, administration of a
ß2AR-selective agonist to NE-depleted mice partially reversed the
suppressed Ab response that resulted from NE depletion. Expression of
the ß2AR on TNP-specific B cells was confirmed by radioligand
binding, immunofluorescence, and cAMP analysis. Also, while splenic
histology was comparable in NE-intact and NE-depleted mice before Ag
exposure, follicle expansion and germinal center formation were
suppressed in NE-depleted mice after Ag exposure. Taken together, these
results suggest that NE stimulation of the ß2AR expressed on B cells
is necessary for the maintenance of an optimal primary and secondary
Th2 cell-dependent Ab response in vivo.
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