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 |
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| Main Authors: | , , , , , , , , |
| 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. |
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| 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 |
| Author_xml | – sequence: 1 givenname: Elizabeth C surname: Nowak fullname: Nowak, Elizabeth C organization: Department of Microbiology and Immunology, Dartmouth Medical School and the Norris Cotton Cancer Center, Lebanon, NH 03756, USA – sequence: 2 givenname: Casey T surname: Weaver fullname: Weaver, Casey T – sequence: 3 givenname: Henrietta surname: Turner fullname: Turner, Henrietta – sequence: 4 givenname: Sakhina surname: Begum-Haque fullname: Begum-Haque, Sakhina – sequence: 5 givenname: Burkhard surname: Becher fullname: Becher, Burkhard – sequence: 6 givenname: Bettina surname: Schreiner fullname: Schreiner, Bettina – sequence: 7 givenname: Anthony J surname: Coyle fullname: Coyle, Anthony J – sequence: 8 givenname: Lloyd H surname: Kasper fullname: Kasper, Lloyd H – sequence: 9 givenname: Randolph J surname: Noelle fullname: Noelle, Randolph J |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19596803$$D View this record in MEDLINE/PubMed |
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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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| 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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