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Published online before print October 29, 2008
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0708394

Received for publication July 1, 2008.
Revised September 22, 2008.
Accepted for publication September 30, 2008.

Article

CCL11 blocks IL-4 and GM-CSF signaling in hematopoietic cells and hinders dendritic cell differentiation via suppressor of cytokine signaling expression

Nigel J. Stevenson *, Mark R. Addley {dagger}, Elizabeth J. Ryan {ddagger}, Caroline R. Boyd *, Helen P. Carroll *, Verica Paunovic *, Christina A. Bursill {dagger}{sect}, Helen C. Miller {dagger}, Keith M. Channon {sect}, Angela E. McClurg *, Marilyn A. Armstrong *, Wilson A. Coulter ||, David R. Greaves {dagger}, and James A. Johnston *@

*Infection and Immunity, Cancer Research and Cell Biology, School of Biomedical Science, and ||School of Dentistry, Queen’s University of Belfast, Belfast, Northern Ireland; {dagger}Sir William Dunn School of Pathology and {sect}Department of Cardiovascular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom; and {ddagger}Department of Immunology and Biochemistry, Trinity College Dublin, Dublin, Ireland

@ To whom correspondence should be addressed. E-mail: Jim.Johnston{at}qub.ac.uk.


  Abstract

The chemokine eotaxin/CCL11 is an important mediator of leukocyte migration, but its effect on inflammatory cytokine signaling has not been explored. In this study, we find that CCL11 induces suppressor of cytokine signaling (SOCS)1 and SOCS3 expression in murine macrophages, human monocytes, and dendritic cells (DCs). We also discover that CCL11 inhibits GM-CSF-mediated STAT5 activation and IL-4-induced STAT6 activation in a range of hematopoietic cells. This blockade of cytokine signaling by CCL11 results in reduced differentiation and endocytic ability of DCs, implicating CCL11-induced SOCS as mediators of chemotactic inflammatory control. These findings demonstrate cross-talk between chemokine and cytokine responses, suggesting that myeloid cells tracking to the inflammatory site do not differentiate in the presence of this chemokine, revealing another role for SOCS in inflammatory regulation.

Key Words: dendritic cells • monocytes/macrophages • chemokines • signal transduction






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