In this paper, we reported that CCR11
is a functional receptor for the MCP family of chemokines. Gosling and
colleagues (Gosling, J., Dairaghi, D. J., Wang, Y., Hanley, M., Talbot,
D., Miao, Z., and Schall, T. J. (2000) J. Immunol. 164, 2851-2856) simultaneously reported ELC, SLC, and TECK to be the
ligands for this receptor (which they called CCR10). Upon further
investigation, the transfected cell line used for our original study
was found to express undetectable levels of CCR11 by Northern analysis.
To generate this cell line, we utilized the selective method of
chemotaxis to enrich for cells that responded to chemokines. The
selected cells responded to MCP-4 and other members of the MCP family
as reported, but new Northern analysis data show an up-regulation of
the endogenous murine CCR2 in these cells. Furthermore, cells
transfected with recombinant murine CCR2 have a ligand recognition
pattern and chemotactic response similar to our reported CCR11.
Consequently, we believe that our observed data were not due to CCR11
but instead may be attributable to up-regulation of the endogenous
murine CCR2 gene. We have since expressed CCR11 in both L1.2 and HEK293 cells and confirmed high levels of expression with a CCR11-specific antiserum. Both cell lines demonstrate binding to ELC, SLC, and TECK.
Therefore, we are in agreement with the results of Gosling et al.
and have confirmed ELC, SLC, and TECK as ligands for CCR11. Other
information in our report regarding the sequence, chromosomal localization, and tissue distribution of the receptor is accurate and
not affected by this correction.