IL-9 as a mediator of Th17-driven inflammatory disease

We report that like other T cells cultured in the presence of transforming growth factor (TGF) beta, Th17 cells also produce interleukin (IL) 9. Th17 cells generated in vitro with IL-6 and TGF-beta as well as purified ex vivo Th17 cells both produced IL-9. To determine if IL-9 has functional consequ...

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Published in:The Journal of experimental medicine Vol. 206; no. 8; p. 1653
Main Authors: Nowak, Elizabeth C, Weaver, Casey T, Turner, Henrietta, Begum-Haque, Sakhina, Becher, Burkhard, Schreiner, Bettina, Coyle, Anthony J, Kasper, Lloyd H, Noelle, Randolph J
Format: Journal Article
Language:English
Published: United States 03.08.2009
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ISSN:1540-9538, 1540-9538
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Abstract We report that like other T cells cultured in the presence of transforming growth factor (TGF) beta, Th17 cells also produce interleukin (IL) 9. Th17 cells generated in vitro with IL-6 and TGF-beta as well as purified ex vivo Th17 cells both produced IL-9. To determine if IL-9 has functional consequences in Th17-mediated inflammatory disease, we evaluated the role of IL-9 in the development and progression of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. The data show that IL-9 neutralization and IL-9 receptor deficiency attenuates disease, and this correlates with decreases in Th17 cells and IL-6-producing macrophages in the central nervous system, as well as mast cell numbers in the regional lymph nodes. Collectively, these data implicate IL-9 as a Th17-derived cytokine that can contribute to inflammatory disease.
AbstractList We report that like other T cells cultured in the presence of transforming growth factor (TGF) beta, Th17 cells also produce interleukin (IL) 9. Th17 cells generated in vitro with IL-6 and TGF-beta as well as purified ex vivo Th17 cells both produced IL-9. To determine if IL-9 has functional consequences in Th17-mediated inflammatory disease, we evaluated the role of IL-9 in the development and progression of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. The data show that IL-9 neutralization and IL-9 receptor deficiency attenuates disease, and this correlates with decreases in Th17 cells and IL-6-producing macrophages in the central nervous system, as well as mast cell numbers in the regional lymph nodes. Collectively, these data implicate IL-9 as a Th17-derived cytokine that can contribute to inflammatory disease.
We report that like other T cells cultured in the presence of transforming growth factor (TGF) beta, Th17 cells also produce interleukin (IL) 9. Th17 cells generated in vitro with IL-6 and TGF-beta as well as purified ex vivo Th17 cells both produced IL-9. To determine if IL-9 has functional consequences in Th17-mediated inflammatory disease, we evaluated the role of IL-9 in the development and progression of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. The data show that IL-9 neutralization and IL-9 receptor deficiency attenuates disease, and this correlates with decreases in Th17 cells and IL-6-producing macrophages in the central nervous system, as well as mast cell numbers in the regional lymph nodes. Collectively, these data implicate IL-9 as a Th17-derived cytokine that can contribute to inflammatory disease.We report that like other T cells cultured in the presence of transforming growth factor (TGF) beta, Th17 cells also produce interleukin (IL) 9. Th17 cells generated in vitro with IL-6 and TGF-beta as well as purified ex vivo Th17 cells both produced IL-9. To determine if IL-9 has functional consequences in Th17-mediated inflammatory disease, we evaluated the role of IL-9 in the development and progression of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. The data show that IL-9 neutralization and IL-9 receptor deficiency attenuates disease, and this correlates with decreases in Th17 cells and IL-6-producing macrophages in the central nervous system, as well as mast cell numbers in the regional lymph nodes. Collectively, these data implicate IL-9 as a Th17-derived cytokine that can contribute to inflammatory disease.
Author Turner, Henrietta
Coyle, Anthony J
Noelle, Randolph J
Weaver, Casey T
Schreiner, Bettina
Nowak, Elizabeth C
Kasper, Lloyd H
Becher, Burkhard
Begum-Haque, Sakhina
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  givenname: Casey T
  surname: Weaver
  fullname: Weaver, Casey T
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  givenname: Henrietta
  surname: Turner
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  givenname: Sakhina
  surname: Begum-Haque
  fullname: Begum-Haque, Sakhina
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  fullname: Noelle, Randolph J
BackLink https://www.ncbi.nlm.nih.gov/pubmed/19596803$$D View this record in MEDLINE/PubMed
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PublicationTitle The Journal of experimental medicine
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PublicationYear 2009
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– reference: 17581588 - Nature. 2007 Jul 26;448(7152):484-7
– reference: 16285014 - Eur J Immunol. 2005 Dec;35(12):3478-86
– reference: 18378796 - J Exp Med. 2008 Apr 14;205(4):897-913
– reference: 17312173 - J Immunol. 2007 Mar 1;178(5):3244-51
– reference: 7517440 - J Neurol Sci. 1994 Apr;122(2):210-3
– reference: 9368607 - Eur J Immunol. 1997 Oct;27(10):2536-40
– reference: 15070693 - Blood. 2004 Apr 15;103(8):3117-21
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Snippet We report that like other T cells cultured in the presence of transforming growth factor (TGF) beta, Th17 cells also produce interleukin (IL) 9. Th17 cells...
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StartPage 1653
SubjectTerms Adoptive Transfer
Animals
Encephalomyelitis, Autoimmune, Experimental - etiology
Encephalomyelitis, Autoimmune, Experimental - immunology
Encephalomyelitis, Autoimmune, Experimental - pathology
Female
In Vitro Techniques
Inflammation Mediators - immunology
Inflammation Mediators - metabolism
Interleukin-9 - antagonists & inhibitors
Interleukin-9 - biosynthesis
Interleukin-9 - immunology
Mice
Mice, Inbred C57BL
Mice, Knockout
Receptors, Interleukin-9 - deficiency
Receptors, Interleukin-9 - genetics
Receptors, Interleukin-9 - immunology
Spinal Cord - immunology
Spinal Cord - pathology
T-Lymphocyte Subsets - classification
T-Lymphocyte Subsets - immunology
T-Lymphocytes, Helper-Inducer - classification
T-Lymphocytes, Helper-Inducer - immunology
Title IL-9 as a mediator of Th17-driven inflammatory disease
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