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CUTTING EDGE |
*
Division of Clinical Immunology and Allergy, Johns Hopkins Asthma and Allergy Center, Baltimore, MD 21224;
Division of Otolaryngology, University of Chicago, Chicago, IL; and
LeukoSite Inc., Boston, MA 02142
Chemokine-induced eosinophil chemotaxis is
mediated primarily through the C-C chemokine receptor, CCR3. We have
now detected CCR3 immunoreactivity on epithelial cells in biopsies of
patients with asthma and other respiratory diseases. CCR3 mRNA was
detected by Northern blot analysis after TNF-
stimulation of the
human primary bronchial epithelial cells as well as the epithelial cell
line, BEAS-2B; IFN-
potentiated the TNF--induced expression.
Western blots and flow cytometry confirmed the expression of CCR3
protein. This receptor is functional based on studies demonstrating
eotaxin-induced intracellular Ca2+ flux and tyrosine
phosphorylation of cellular proteins. The specificity
of this functional response was confirmed by blocking these signaling
events with anti-CCR3 mAb (7B11) or pertussis toxin. Furthermore,
125I-eotaxin binding assay confirmed that CCR3 expressed on
epithelial cells have the expected ligand specificity. These studies
indicate that airway epithelial cells express CCR3 and suggest that
CCR3 ligands may influence epithelial cell
functions.
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