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1b-Adrenergic Receptors1
Center for Experimental Pathology, Istituto Cantonale di Patologia, Locarno, Switzerland
Dendritic cells (DC) bring Ags into lymphoid organs via lymphatic
vessels. In this study, we investigated the possibility that the
sympathetic neurotransmitter norepinephrine (NE) influences DC
migration. Murine epidermal Langerhans cells mobilization is enhanced
by systemic treatment with the 
2-adrenergic antagonist
yohimbine and inhibited by local treatment with the specific
1-adrenergic antagonist prazosin (PRA). Consistently, NE
enhances spontaneous emigration of DC from ear skin explants, and PRA
inhibits this effect. In addition, local treatment with PRA during
sensitization with FITC inhibits the contact hypersensitivity response
6 days later. In vitro, bone marrow-derived immature, but not
CD40-stimulated mature DC migrate in response to NE, and this effect is
neutralized by PRA. NE seems to exert both a chemotactic and
chemokinetic activity on immature DC. Coherently, immature, but not
mature DC, express mRNA coding for the 1b-adrenergic
receptor subtype. Inactivation of this adrenergic receptor by the
specific and irreversible antagonist chloroethylclonidine hinders the
migration of injected DC from the footpad to regional lymph nodes.
Thus, besides regulating lymph flow, the sympathetic innervation of
lymphatic vessels may participate in directing DC migration from the
site of inflammation to regional lymph nodes. Alternatively, the
chemokinetic activity of NE may enhance the ability of DC to sample
local Ags, and hence increase the number of DC migrating to the
draining lymph nodes. This finding might improve our understanding of
the biological basis of skin diseases and allergic reactions, and opens
new pharmacological possibilities to modulate the immune
response.
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