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; Elizabeth J. Ryan; Caroline R. Boyd; Helen P. Carroll; Verica Paunovic; Christina A. Bursill; Helen C. Miller; Keith M. Channon; Angela E. McClurg; Marilyn A. Armstrong; Wilson A. Coulter; David R. Greaves; James A. Johnston

doi:10.1189/jlb.0708394

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, Elizabeth J. Ryan, Caroline R. Boyd, Helen P. Carroll, Verica Paunovic, Christina A. Bursill, Helen C. Miller, Keith M. Channon, Angela E. McClurg, Marilyn A. Armstrong, Wilson A. Coulter, David R. Greaves, James A. Johnston

Research output: Contribution to journal › Article › peer-review

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 chemo-kine 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.

Original language	English
Pages (from-to)	289-297
Number of pages	9
Journal	Journal of Leukocyte Biology
Volume	85
Issue number	2
DOIs	https://doi.org/10.1189/jlb.0708394
Publication status	Published - 1 Feb 2009
Externally published	Yes

Keywords

Chemokines
Dendritic cells
Monocytes/macrophages
Signal transduction

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1189/jlb.0708394

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Stevenson, N. J., Addley, M. R., Ryan, E. J., Boyd, C. R., Carroll, H. P., Paunovic, V., Bursill, C. A., Miller, H. C., Channon, K. M., McClurg, A. E., Armstrong, M. A., Coulter, W. A., Greaves, D. R., & Johnston, J. A. (2009). CCL11 blocks IL-4 and GM-CSF signaling in hematopoietic cells and hinders dendritic cell differentiation via suppressor of cytokine signaling expression. Journal of Leukocyte Biology, 85(2), 289-297. https://doi.org/10.1189/jlb.0708394

@article{08cf341284544d91bf285b83aec847c6,

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

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 chemo-kine 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.",

keywords = "Chemokines, Dendritic cells, Monocytes/macrophages, Signal transduction",

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

year = "2009",

month = feb,

day = "1",

doi = "10.1189/jlb.0708394",

language = "English",

volume = "85",

pages = "289--297",

journal = "Journal of Leukocyte Biology",

issn = "0741-5400",

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}

Stevenson, NJ, Addley, MR, Ryan, EJ, Boyd, CR, Carroll, HP, Paunovic, V, Bursill, CA, Miller, HC, Channon, KM, McClurg, AE, Armstrong, MA, Coulter, WA, Greaves, DR & Johnston, JA 2009, 'CCL11 blocks IL-4 and GM-CSF signaling in hematopoietic cells and hinders dendritic cell differentiation via suppressor of cytokine signaling expression', Journal of Leukocyte Biology, vol. 85, no. 2, pp. 289-297. https://doi.org/10.1189/jlb.0708394

TY - JOUR

T1 - CCL11 blocks IL-4 and GM-CSF signaling in hematopoietic cells and hinders dendritic cell differentiation via suppressor of cytokine signaling expression

AU - Stevenson, Nigel J.

AU - Addley, Mark R.

AU - Ryan, Elizabeth J.

AU - Boyd, Caroline R.

AU - Carroll, Helen P.

AU - Paunovic, Verica

AU - Bursill, Christina A.

AU - Miller, Helen C.

AU - Channon, Keith M.

AU - McClurg, Angela E.

AU - Armstrong, Marilyn A.

AU - Coulter, Wilson A.

AU - Greaves, David R.

AU - Johnston, James A.

PY - 2009/2/1

Y1 - 2009/2/1

N2 - 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 chemo-kine 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.

AB - 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 chemo-kine 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.

KW - Chemokines

KW - Dendritic cells

KW - Monocytes/macrophages

KW - Signal transduction

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U2 - 10.1189/jlb.0708394

DO - 10.1189/jlb.0708394

M3 - Article

C2 - 18971287

AN - SCOPUS:59649114146

SN - 0741-5400

VL - 85

SP - 289

EP - 297

JO - Journal of Leukocyte Biology

JF - Journal of Leukocyte Biology

IS - 2

ER -

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

Abstract

Keywords

UN SDGs

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