General nature of the STAT3-activated anti-inflammatory response

Karim C. El Kasmi; Jeff Holst; Maryaline Coffre; Lisa Mielke; Antoine De Pauw; Nouara Lhocine; Amber M. Smith; Robert Rutschman; Deepak Kaushal; Yuhong Shen; Takashi Suda; Raymond P. Donnelly; Martin G. Myers; Warren Alexander; Dario A.A. Vignali; Stephanie S. Watowich; Matthias Ernst; Douglas J. Hilton; Peter J. Murray

doi:10.4049/jimmunol.177.11.7880

General nature of the STAT3-activated anti-inflammatory response

Karim C. El Kasmi, Jeff Holst, Maryaline Coffre, Lisa Mielke, Antoine De Pauw, Nouara Lhocine, Amber M. Smith, Robert Rutschman, Deepak Kaushal, Yuhong Shen, Takashi Suda, Raymond P. Donnelly, Martin G. Myers, Warren Alexander, Dario A.A. Vignali, Stephanie S. Watowich, Matthias Ernst, Douglas J. Hilton, Peter J. Murray

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

188 Citations (Scopus)

Abstract

Although many cytokine receptors generate their signals via the STAT3 pathway, the IL-10R appears unique in promoting a potent anti-inflammatory response (AIR) via STAT3 to antagonize proinflammatory signals that activate the innate immune response. We found that heterologous cytokine receptor systems that activate STAT3 but are naturally refractory (the IL-22R), or engineered to be refractory (the IL-6, leptin, and erythropoietin receptors), to suppressor of cytokine signaling-3-mediated inhibition activate an AIR indistinguishable from IL-10. We conclude that the AIR is a generic cytokine signaling pathway dependent on STAT3 but not unique to the IL-10R.

Original language	English
Pages (from-to)	7880-7888
Number of pages	9
Journal	Journal of Immunology
Volume	177
Issue number	11
DOIs	https://doi.org/10.4049/jimmunol.177.11.7880
Publication status	Published - 1 Dec 2006
Externally published	Yes

Access to Document

10.4049/jimmunol.177.11.7880

Cite this

El Kasmi, K. C., Holst, J., Coffre, M., Mielke, L., De Pauw, A., Lhocine, N., Smith, A. M., Rutschman, R., Kaushal, D., Shen, Y., Suda, T., Donnelly, R. P., Myers, M. G., Alexander, W., Vignali, D. A. A., Watowich, S. S., Ernst, M., Hilton, D. J., & Murray, P. J. (2006). General nature of the STAT3-activated anti-inflammatory response. Journal of Immunology, 177(11), 7880-7888. https://doi.org/10.4049/jimmunol.177.11.7880

@article{b355caad4bcb421e8637489e1f336c12,

title = "General nature of the STAT3-activated anti-inflammatory response",

abstract = "Although many cytokine receptors generate their signals via the STAT3 pathway, the IL-10R appears unique in promoting a potent anti-inflammatory response (AIR) via STAT3 to antagonize proinflammatory signals that activate the innate immune response. We found that heterologous cytokine receptor systems that activate STAT3 but are naturally refractory (the IL-22R), or engineered to be refractory (the IL-6, leptin, and erythropoietin receptors), to suppressor of cytokine signaling-3-mediated inhibition activate an AIR indistinguishable from IL-10. We conclude that the AIR is a generic cytokine signaling pathway dependent on STAT3 but not unique to the IL-10R.",

author = "{El Kasmi}, {Karim C.} and Jeff Holst and Maryaline Coffre and Lisa Mielke and {De Pauw}, Antoine and Nouara Lhocine and Smith, {Amber M.} and Robert Rutschman and Deepak Kaushal and Yuhong Shen and Takashi Suda and Donnelly, {Raymond P.} and Myers, {Martin G.} and Warren Alexander and Vignali, {Dario A.A.} and Watowich, {Stephanie S.} and Matthias Ernst and Hilton, {Douglas J.} and Murray, {Peter J.}",

year = "2006",

month = dec,

day = "1",

doi = "10.4049/jimmunol.177.11.7880",

language = "English",

volume = "177",

pages = "7880--7888",

journal = "Journal of Immunology",

issn = "0022-1767",

publisher = "American Association of Immunologists",

number = "11",

}

El Kasmi, KC, Holst, J, Coffre, M, Mielke, L, De Pauw, A, Lhocine, N, Smith, AM, Rutschman, R, Kaushal, D, Shen, Y, Suda, T, Donnelly, RP, Myers, MG, Alexander, W, Vignali, DAA, Watowich, SS, Ernst, M, Hilton, DJ & Murray, PJ 2006, 'General nature of the STAT3-activated anti-inflammatory response', Journal of Immunology, vol. 177, no. 11, pp. 7880-7888. https://doi.org/10.4049/jimmunol.177.11.7880

TY - JOUR

T1 - General nature of the STAT3-activated anti-inflammatory response

AU - El Kasmi, Karim C.

AU - Holst, Jeff

AU - Coffre, Maryaline

AU - Mielke, Lisa

AU - De Pauw, Antoine

AU - Lhocine, Nouara

AU - Smith, Amber M.

AU - Rutschman, Robert

AU - Kaushal, Deepak

AU - Shen, Yuhong

AU - Suda, Takashi

AU - Donnelly, Raymond P.

AU - Myers, Martin G.

AU - Alexander, Warren

AU - Vignali, Dario A.A.

AU - Watowich, Stephanie S.

AU - Ernst, Matthias

AU - Hilton, Douglas J.

AU - Murray, Peter J.

PY - 2006/12/1

Y1 - 2006/12/1

N2 - Although many cytokine receptors generate their signals via the STAT3 pathway, the IL-10R appears unique in promoting a potent anti-inflammatory response (AIR) via STAT3 to antagonize proinflammatory signals that activate the innate immune response. We found that heterologous cytokine receptor systems that activate STAT3 but are naturally refractory (the IL-22R), or engineered to be refractory (the IL-6, leptin, and erythropoietin receptors), to suppressor of cytokine signaling-3-mediated inhibition activate an AIR indistinguishable from IL-10. We conclude that the AIR is a generic cytokine signaling pathway dependent on STAT3 but not unique to the IL-10R.

AB - Although many cytokine receptors generate their signals via the STAT3 pathway, the IL-10R appears unique in promoting a potent anti-inflammatory response (AIR) via STAT3 to antagonize proinflammatory signals that activate the innate immune response. We found that heterologous cytokine receptor systems that activate STAT3 but are naturally refractory (the IL-22R), or engineered to be refractory (the IL-6, leptin, and erythropoietin receptors), to suppressor of cytokine signaling-3-mediated inhibition activate an AIR indistinguishable from IL-10. We conclude that the AIR is a generic cytokine signaling pathway dependent on STAT3 but not unique to the IL-10R.

UR - http://www.scopus.com/inward/record.url?scp=33751555600&partnerID=8YFLogxK

U2 - 10.4049/jimmunol.177.11.7880

DO - 10.4049/jimmunol.177.11.7880

M3 - Article

C2 - 17114459

AN - SCOPUS:33751555600

SN - 0022-1767

VL - 177

SP - 7880

EP - 7888

JO - Journal of Immunology

JF - Journal of Immunology

IS - 11

ER -

General nature of the STAT3-activated anti-inflammatory response

Abstract

Access to Document

Other files and links

Cite this