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*
Tokyo Research Laboratories, Kyowa Hakko Kogyo, Tokyo, Japan; and
Toxicological Research Laboratories, Kyowa Hakko Kogyo, Yamaguchi, Japan
IL-4 has been shown to be involved in the accumulation of
leukocytes, especially eosinophils, at sites of inflammation by acting
on vascular endothelial cells. To identify novel molecules involved in
the IL-4-dependent eosinophil extravasation, cDNA prepared from HUVEC
stimulated with IL-4 was subjected to differential display analysis,
which revealed a novel CC chemokine designated as eotaxin-3. The human
eotaxin-3 gene has been localized to chromosome 7q11.2, unlike most
other CC chemokine genes. The predicted mature protein of 71 aa showed
27–42% identity to other human CC chemokines. The recombinant protein
induced a transient increase in the cytosolic Ca2+
concentration and in vitro chemotaxis on eosinophils. Furthermore, in
cynomolgus monkeys, the accumulation of eosinophils was observed at the
sites where the protein was injected. Eotaxin-3 inhibited the binding
of 125I-eotaxin, but not 125I-macrophage
inflammatory protein-1
, to eosinophils and acted on cell lines
transfected with CCR-3, suggesting that eotaxin-3 recognized CCR-3.
IL-13 as well as IL-4 up-regulated eotaxin-3 mRNA in HUVEC, whereas
neither TNF-, IL-1
, IFN-
, nor TNF- plus IFN- did. The
expression profile of eotaxin-3 is different from those of eotaxin,
RANTES, and monocyte chemoattractant protein-4, which are potent
eosinophil-selective chemoattractants and are induced by either TNF-
or TNF- plus IFN-. These results suggest that eotaxin-3 may
contribute to the eosinophil accumulation in atopic
diseases.
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