MicroRNA-21 promotes Th17 differentiation and mediates experimental autoimmune encephalomyelitis

Accumulation of IL-17-producing Th17 cells is associated with the development of multiple autoimmune diseases; however, the contribution of microRNA (miRNA) pathways to the intrinsic control of Th17 development remains unclear. Here, we demonstrated that miR-21 expression is elevated in Th17 cells a...

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Vydáno v:	The Journal of clinical investigation Ročník 125; číslo 3; s. 1069 - 1080
Hlavní autoři:	Murugaiyan, Gopal, da Cunha, Andre Pires, Ajay, Amrendra K., Joller, Nicole, Garo, Lucien P., Kumaradevan, Sowmiya, Yosef, Nir, Vaidya, Vishal S., Weiner, Howard L.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States American Society for Clinical Investigation 01.03.2015
Témata:	Animals Autoimmune diseases Base Sequence Binding Sites Biomedical research Care and treatment Cell Differentiation Cells, Cultured Encephalomyelitis Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Female Gene Expression Hospitals Immune system Interleukin-17 - genetics Interleukin-17 - metabolism Lymphocytes Mice, Inbred C57BL MicroRNA MicroRNAs - physiology Physiological aspects Rheumatology RNA Interference Smad7 Protein - genetics Smad7 Protein - metabolism Studies Th17 Cells - physiology Transcription factors
ISSN:	0021-9738, 1558-8238, 1558-8238
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Abstract	Accumulation of IL-17-producing Th17 cells is associated with the development of multiple autoimmune diseases; however, the contribution of microRNA (miRNA) pathways to the intrinsic control of Th17 development remains unclear. Here, we demonstrated that miR-21 expression is elevated in Th17 cells and that mice lacking miR-21 have a defect in Th17 differentiation and are resistant to experimental autoimmune encephalomyelitis (EAE). Furthermore, we determined that miR-21 promotes Th17 differentiation by targeting and depleting SMAD-7, a negative regulator of TGF-β signaling. Moreover, the decreases in Th17 differentiation in miR-21-deficient T cells were associated with defects in SMAD-2/3 activation and IL-2 suppression. Finally, we found that treatment of WT mice with an anti-miR-21 oligonucleotide reduced the clinical severity of EAE, which was associated with a decrease in Th17 cells. Thus, we have characterized a T cell-intrinsic miRNA pathway that enhances TGF-β signaling, limits the autocrine inhibitory effects of IL-2, and thereby promotes Th17 differentiation and autoimmunity.
AbstractList	Accumulation of IL-17-producing Th17 cells is associated with the development of multiple autoimmune diseases; however, the contribution of microRNA (miRNA) pathways to the intrinsic control of Th17 development remains unclear. Here, we demonstrated that miR-21 expression is elevated in Th17 cells and that mice lacking miR-21 have a defect in Th17 differentiation and are resistant to experimental autoimmune encephalomyelitis (EAE). Furthermore, we determined that miR-21 promotes Th17 differentiation by targeting and depleting SMAD-7, a negative regulator of TGF-β signaling. Moreover, the decreases in Th17 differentiation in miR-21-deficient T cells were associated with defects in SMAD-2/3 activation and IL-2 suppression. Finally, we found that treatment of WT mice with an anti-miR-21 oligonucleotide reduced the clinical severity of EAE, which was associated with a decrease in Th17 cells. Thus, we have characterized a T cell-intrinsic miRNA pathway that enhances TGF-β signaling, limits the autocrine inhibitory effects of IL-2, and thereby promotes Th17 differentiation and autoimmunity. Accumulation of IL-17-producing Th17 cells is associated with the development of multiple autoimmune diseases; however, the contribution of microRNA (miRNA) pathways to the intrinsic control of Th17 development remains unclear. Here, we demonstrated that miR-21 expression is elevated in Th17 cells and that mice lacking miR-21 have a defect in Th17 differentiation and are resistant to experimental autoimmune encephalomyelitis (EAE). Furthermore, we determined that miR-21 promotes Th17 differentiation by targeting and depleting SMAD-7, a negative regulator of TGF- beta signaling. Moreover, the decreases in Th17 differentiation in miR-21-deficient T cells were associated with defects in SMAD-2/3 activation and IL-2 suppression. Finally, we found that treatment of WT mice with an anti-miR-21 oligonucleotide reduced the clinical severity of EAE, which was associated with a decrease in Th17 cells. Thus, we have characterized a T cell-intrinsic miRNA pathway that enhances TGF- beta signaling, limits the autocrine inhibitory effects of IL-2, and thereby promotes Th17 differentiation and autoimmunity. Accumulation of IL-17-producing Th17 cells is associated with the development of multiple autoimmune diseases; however, the contribution of microRNA (miRNA) pathways to the intrinsic control of Th17 development remains unclear. Here, we demonstrated that miR-21 expression is elevated in Th17 cells and that mice lacking miR-21 have a defect in Th17 differentiation and are resistant to experimental autoimmune encephalomyelitis (EAE). Furthermore, we determined that miR-21 promotes Th17 differentiation by targeting and depleting SMAD-7, a negative regulator of TGF-β signaling. Moreover, the decreases in Th17 differentiation in miR-21-deficient T cells were associated with defects in SMAD-2/3 activation and IL-2 suppression. Finally, we found that treatment of WT mice with an anti-miR-21 oligonucleotide reduced the clinical severity of EAE, which was associated with a decrease in Th17 cells. Thus, we have characterized a T cell-intrinsic miRNA pathway that enhances TGF-β signaling, limits the autocrine inhibitory effects of IL-2, and thereby promotes Th17 differentiation and autoimmunity.Accumulation of IL-17-producing Th17 cells is associated with the development of multiple autoimmune diseases; however, the contribution of microRNA (miRNA) pathways to the intrinsic control of Th17 development remains unclear. Here, we demonstrated that miR-21 expression is elevated in Th17 cells and that mice lacking miR-21 have a defect in Th17 differentiation and are resistant to experimental autoimmune encephalomyelitis (EAE). Furthermore, we determined that miR-21 promotes Th17 differentiation by targeting and depleting SMAD-7, a negative regulator of TGF-β signaling. Moreover, the decreases in Th17 differentiation in miR-21-deficient T cells were associated with defects in SMAD-2/3 activation and IL-2 suppression. Finally, we found that treatment of WT mice with an anti-miR-21 oligonucleotide reduced the clinical severity of EAE, which was associated with a decrease in Th17 cells. Thus, we have characterized a T cell-intrinsic miRNA pathway that enhances TGF-β signaling, limits the autocrine inhibitory effects of IL-2, and thereby promotes Th17 differentiation and autoimmunity.
Audience	Academic
Author	Joller, Nicole Vaidya, Vishal S. Murugaiyan, Gopal da Cunha, Andre Pires Weiner, Howard L. Garo, Lucien P. Kumaradevan, Sowmiya Ajay, Amrendra K. Yosef, Nir
AuthorAffiliation	2 Evergrande Center for Immunologic Diseases, and 4 Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland 3 Renal Division, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA 1 Ann Romney Center for Neurologic Diseases 5 Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA
AuthorAffiliation_xml	– name: 1 Ann Romney Center for Neurologic Diseases – name: 5 Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA – name: 2 Evergrande Center for Immunologic Diseases, and – name: 3 Renal Division, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA – name: 4 Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland
Author_xml	– sequence: 1 givenname: Gopal surname: Murugaiyan fullname: Murugaiyan, Gopal – sequence: 2 givenname: Andre Pires surname: da Cunha fullname: da Cunha, Andre Pires – sequence: 3 givenname: Amrendra K. surname: Ajay fullname: Ajay, Amrendra K. – sequence: 4 givenname: Nicole surname: Joller fullname: Joller, Nicole – sequence: 5 givenname: Lucien P. surname: Garo fullname: Garo, Lucien P. – sequence: 6 givenname: Sowmiya surname: Kumaradevan fullname: Kumaradevan, Sowmiya – sequence: 7 givenname: Nir surname: Yosef fullname: Yosef, Nir – sequence: 8 givenname: Vishal S. surname: Vaidya fullname: Vaidya, Vishal S. – sequence: 9 givenname: Howard L. surname: Weiner fullname: Weiner, Howard L.
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/25642768$$D View this record in MEDLINE/PubMed
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Snippet	Accumulation of IL-17-producing Th17 cells is associated with the development of multiple autoimmune diseases; however, the contribution of microRNA (miRNA)... Accumulation of IL-17–producing Th17 cells is associated with the development of multiple autoimmune diseases; however, the contribution of microRNA (miRNA)...
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SubjectTerms	Animals Autoimmune diseases Base Sequence Binding Sites Biomedical research Care and treatment Cell Differentiation Cells, Cultured Encephalomyelitis Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Female Gene Expression Hospitals Immune system Interleukin-17 - genetics Interleukin-17 - metabolism Lymphocytes Mice, Inbred C57BL MicroRNA MicroRNAs - physiology Physiological aspects Rheumatology RNA Interference Smad7 Protein - genetics Smad7 Protein - metabolism Studies Th17 Cells - physiology Transcription factors
Title	MicroRNA-21 promotes Th17 differentiation and mediates experimental autoimmune encephalomyelitis
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