CCL11 blocks IL-4 and GM-CSF signaling in hematopoietic cells and hinders dendritic cell differentiation via suppressor of cytokine signaling expression
Autor: | Mark R. Addley, Nigel J. Stevenson, Caroline R. Boyd, Verica Paunovic, Wilson A. Coulter, Keith M. Channon, Christina A. Bursill, James A. Johnston, Marilyn A. Armstrong, Angela McClurg, Elizabeth J. Ryan, David R. Greaves, Helen P. Carroll, Helen C. Miller |
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Jazyk: | angličtina |
Rok vydání: | 2016 |
Předmět: |
Chemokine CCL11
Hematopoietic System Immunology Suppressor of Cytokine Signaling Proteins GTP-Binding Protein alpha Subunits Gi-Go Biology Suppressor of cytokine signalling Cell Line Receptors G-Protein-Coupled Mice Suppressor of Cytokine Signaling 1 Protein Animals Humans Immunology and Allergy CXCL10 SOCS5 SOCS3 CXCL14 Suppressor of cytokine signaling 1 Macrophages Granulocyte-Macrophage Colony-Stimulating Factor Cell Differentiation Dendritic Cells Cell Biology respiratory system Endocytosis Cell biology Mice Inbred C57BL CXCL2 Suppressor of Cytokine Signaling 3 Protein Cytokines Interleukin-4 Inflammation Mediators CCL25 Signal Transduction |
DOI: | 10.1189/jlb.0708394 |
Popis: | 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. |
Databáze: | OpenAIRE |
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