microRNA-92a promotes CNS autoimmunity by modulating the regulatory and inflammatory T cell balance
A disequilibrium between immunosuppressive Tregs and inflammatory IL-17-producing Th17 cells is a hallmark of autoimmune diseases, including multiple sclerosis (MS). However, the molecular mechanisms underlying the Treg and Th17 imbalance in CNS autoimmunity remain largely unclear. Identifying the f...
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| Published in: | The Journal of clinical investigation Vol. 132; no. 10; pp. 1 - 16 |
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| Main Authors: | , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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American Society for Clinical Investigation
16.05.2022
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| ISSN: | 1558-8238, 0021-9738, 1558-8238 |
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| Abstract | A disequilibrium between immunosuppressive Tregs and inflammatory IL-17-producing Th17 cells is a hallmark of autoimmune diseases, including multiple sclerosis (MS). However, the molecular mechanisms underlying the Treg and Th17 imbalance in CNS autoimmunity remain largely unclear. Identifying the factors that drive this imbalance is of high clinical interest. Here, we report a major disease-promoting role for microRNA-92a (miR-92a) in CNS autoimmunity. miR-92a was elevated in experimental autoimmune encephalomyelitis (EAE), and its loss attenuated EAE. Mechanistically, miR-92a mediated EAE susceptibility in a T cell-intrinsic manner by restricting Treg induction and suppressive capacity, while supporting Th17 responses, by directly repressing the transcription factor Foxo1. Although miR-92a did not directly alter Th1 differentiation, it appeared to indirectly promote Th1 cells by inhibiting Treg responses. Correspondingly, miR-92a inhibitor therapy ameliorated EAE by concomitantly boosting Treg responses and dampening inflammatory T cell responses. Analogous to our findings in mice, miR-92a was elevated in CD4+ T cells from patients with MS, and miR-92a silencing in patients' T cells promoted Treg development but limited Th17 differentiation. Together, our results demonstrate that miR-92a drives CNS autoimmunity by sustaining the Treg/Th17 imbalance and implicate miR-92a as a potential therapeutic target for MS. |
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| AbstractList | A disequilibrium between immunosuppressive Tregs and inflammatory IL-17- producing Th17 cells is a hallmark of autoimmune diseases, including multiple sclerosis (MS). However, the molecular mechanisms underlying the Treg and Th17 imbalance in CNS autoimmunity remain largely unclear. Identifying the factors that drive this imbalance is of high clinical interest. Here, we report a major disease-promoting role for microRNA-92a (miR- 92a) in CNS autoimmunity. miR-92a was elevated in experimental autoimmune encephalomyelitis (EAE), and its loss attenuated EAE. Mechanistically, miR92a mediated EAE susceptibility in a T cell-intrinsic manner by restricting Treg induction and suppressive capacity, while supporting Th17 responses, by directly repressing the transcription factor Foxo1. Although miR-92a did not directly alter Th1 differentiation, it appeared to indirectly promote Th1 cells by inhibiting Treg responses. Correspondingly, miR-92a inhibitor therapy ameliorated EAE by concomitantly boosting Treg responses and dampening inflammatory T cell responses. Analogous to our findings in mice, miR-92a was elevated in [CD4.sup.+] T cells from patients with MS, and miR-92a silencing in patients' T cells promoted Treg development but limited Th17 differentiation. Together, our results demonstrate that miR-92a drives CNS autoimmunity by sustaining the Treg/Th17 imbalance and implicate miR-92a as a potential therapeutic target for MS. A disequilibrium between immunosuppressive Tregs and inflammatory IL-17-producing Th17 cells is a hallmark of autoimmune diseases, including multiple sclerosis (MS). However, the molecular mechanisms underlying the Treg and Th17 imbalance in CNS autoimmunity remain largely unclear. Identifying the factors that drive this imbalance is of high clinical interest. Here, we report a major disease-promoting role for microRNA-92a (miR-92a) in CNS autoimmunity. miR-92a was elevated in experimental autoimmune encephalomyelitis (EAE), and its loss attenuated EAE. Mechanistically, miR-92a mediated EAE susceptibility in a T cell-intrinsic manner by restricting Treg induction and suppressive capacity, while supporting Th17 responses, by directly repressing the transcription factor Foxo1. Although miR-92a did not directly alter Th1 differentiation, it appeared to indirectly promote Th1 cells by inhibiting Treg responses. Correspondingly, miR-92a inhibitor therapy ameliorated EAE by concomitantly boosting Treg responses and dampening inflammatory T cell responses. Analogous to our findings in mice, miR-92a was elevated in CD4+ T cells from patients with MS, and miR-92a silencing in patients' T cells promoted Treg development but limited Th17 differentiation. Together, our results demonstrate that miR-92a drives CNS autoimmunity by sustaining the Treg/Th17 imbalance and implicate miR-92a as a potential therapeutic target for MS.A disequilibrium between immunosuppressive Tregs and inflammatory IL-17-producing Th17 cells is a hallmark of autoimmune diseases, including multiple sclerosis (MS). However, the molecular mechanisms underlying the Treg and Th17 imbalance in CNS autoimmunity remain largely unclear. Identifying the factors that drive this imbalance is of high clinical interest. Here, we report a major disease-promoting role for microRNA-92a (miR-92a) in CNS autoimmunity. miR-92a was elevated in experimental autoimmune encephalomyelitis (EAE), and its loss attenuated EAE. Mechanistically, miR-92a mediated EAE susceptibility in a T cell-intrinsic manner by restricting Treg induction and suppressive capacity, while supporting Th17 responses, by directly repressing the transcription factor Foxo1. Although miR-92a did not directly alter Th1 differentiation, it appeared to indirectly promote Th1 cells by inhibiting Treg responses. Correspondingly, miR-92a inhibitor therapy ameliorated EAE by concomitantly boosting Treg responses and dampening inflammatory T cell responses. Analogous to our findings in mice, miR-92a was elevated in CD4+ T cells from patients with MS, and miR-92a silencing in patients' T cells promoted Treg development but limited Th17 differentiation. Together, our results demonstrate that miR-92a drives CNS autoimmunity by sustaining the Treg/Th17 imbalance and implicate miR-92a as a potential therapeutic target for MS. A disequilibrium between immunosuppressive Tregs and inflammatory IL-17–producing Th17 cells is a hallmark of autoimmune diseases, including multiple sclerosis (MS). However, the molecular mechanisms underlying the Treg and Th17 imbalance in CNS autoimmunity remain largely unclear. Identifying the factors that drive this imbalance is of high clinical interest. Here, we report a major disease-promoting role for microRNA-92a (miR-92a) in CNS autoimmunity. miR-92a was elevated in experimental autoimmune encephalomyelitis (EAE), and its loss attenuated EAE. Mechanistically, miR-92a mediated EAE susceptibility in a T cell–intrinsic manner by restricting Treg induction and suppressive capacity, while supporting Th17 responses, by directly repressing the transcription factor Foxo1. Although miR-92a did not directly alter Th1 differentiation, it appeared to indirectly promote Th1 cells by inhibiting Treg responses. Correspondingly, miR-92a inhibitor therapy ameliorated EAE by concomitantly boosting Treg responses and dampening inflammatory T cell responses. Analogous to our findings in mice, miR-92a was elevated in CD4+ T cells from patients with MS, and miR-92a silencing in patients’ T cells promoted Treg development but limited Th17 differentiation. Together, our results demonstrate that miR-92a drives CNS autoimmunity by sustaining the Treg/Th17 imbalance and implicate miR-92a as a potential therapeutic target for MS. A disequilibrium between immunosuppressive Tregs and inflammatory IL-17-producing Th17 cells is a hallmark of autoimmune diseases, including multiple sclerosis (MS). However, the molecular mechanisms underlying the Treg and Th17 imbalance in CNS autoimmunity remain largely unclear. Identifying the factors that drive this imbalance is of high clinical interest. Here, we report a major disease-promoting role for microRNA-92a (miR-92a) in CNS autoimmunity. miR-92a was elevated in experimental autoimmune encephalomyelitis (EAE), and its loss attenuated EAE. Mechanistically, miR92a mediated EAE susceptibility in a T cell-intrinsic manner by restricting Treg induction and suppressive capacity, while supporting Th17 responses, by directly repressing the transcription factor Foxo1. Although miR-92a did not directly alter Th1 differentiation, it appeared to indirectly promote Th1 cells by inhibiting Treg responses. Correspondingly, miR-92a inhibitor therapy ameliorated EAE by concomitantly boosting Treg responses and dampening inflammatory T cell responses. Analogous to our findings in mice, miR-92a was elevated in CD4+ T cells from patients with MS, and miR-92a silencing in patients' T cells promoted Treg development but limited Th17 differentiation. Together, our results demonstrate that miR-92a drives CNS autoimmunity by sustaining the Treg/Th17 imbalance and implicate miR-92a as a potential therapeutic target for MS. |
| Audience | Academic |
| Author | Gabriely, Galina Gandhi, Roopali Fujiwara, Mai Beynon, Vanessa Chitnis, Tanuja Murugaiyan, Gopal Garo, Lucien P. Ajay, Amrendra K. Karandikar, Sukrut H. Raheja, Radhika Hu, Dan Krishnan, Rajesh Weiner, Howard L. Patel, Amee Saxena, Shrishti Healy, Brian C. Paul, Anu Kadowaki-Saga, Ryoko |
| AuthorAffiliation | 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, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA 2 Pulmonary Center, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA |
| AuthorAffiliation_xml | – name: 2 Pulmonary Center, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA – name: 3 Renal Division, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA – name: 1 Ann Romney Center for Neurologic Diseases, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA |
| Author_xml | – sequence: 1 givenname: Mai orcidid: 0000-0001-5540-182X surname: Fujiwara fullname: Fujiwara, Mai – sequence: 2 givenname: Radhika surname: Raheja fullname: Raheja, Radhika – sequence: 3 givenname: Lucien P. surname: Garo fullname: Garo, Lucien P. – sequence: 4 givenname: Amrendra K. orcidid: 0000-0003-2790-5726 surname: Ajay fullname: Ajay, Amrendra K. – sequence: 5 givenname: Ryoko surname: Kadowaki-Saga fullname: Kadowaki-Saga, Ryoko – sequence: 6 givenname: Sukrut H. surname: Karandikar fullname: Karandikar, Sukrut H. – sequence: 7 givenname: Galina surname: Gabriely fullname: Gabriely, Galina – sequence: 8 givenname: Rajesh surname: Krishnan fullname: Krishnan, Rajesh – sequence: 9 givenname: Vanessa surname: Beynon fullname: Beynon, Vanessa – sequence: 10 givenname: Anu surname: Paul fullname: Paul, Anu – sequence: 11 givenname: Amee surname: Patel fullname: Patel, Amee – sequence: 12 givenname: Shrishti orcidid: 0000-0003-3429-5671 surname: Saxena fullname: Saxena, Shrishti – sequence: 13 givenname: Dan surname: Hu fullname: Hu, Dan – sequence: 14 givenname: Brian C. surname: Healy fullname: Healy, Brian C. – sequence: 15 givenname: Tanuja surname: Chitnis fullname: Chitnis, Tanuja – sequence: 16 givenname: Roopali surname: Gandhi fullname: Gandhi, Roopali – sequence: 17 givenname: Howard L. surname: Weiner fullname: Weiner, Howard L. – sequence: 18 givenname: Gopal orcidid: 0000-0003-0439-1363 surname: Murugaiyan fullname: Murugaiyan, Gopal |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35298438$$D View this record in MEDLINE/PubMed |
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| Copyright | COPYRIGHT 2022 American Society for Clinical Investigation Copyright American Society for Clinical Investigation May 2022 2022 Fujiwara et al. 2022 Fujiwara et al. |
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| Keywords | Autoimmunity Multiple sclerosis Inflammation Autoimmune diseases T cells |
| Language | English |
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| Snippet | A disequilibrium between immunosuppressive Tregs and inflammatory IL-17-producing Th17 cells is a hallmark of autoimmune diseases, including multiple sclerosis... A disequilibrium between immunosuppressive Tregs and inflammatory IL-17- producing Th17 cells is a hallmark of autoimmune diseases, including multiple... A disequilibrium between immunosuppressive Tregs and inflammatory IL-17–producing Th17 cells is a hallmark of autoimmune diseases, including multiple sclerosis... |
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| SubjectTerms | Animals Autoimmune diseases Autoimmunity Biomedical research CD4 antigen Cell Differentiation Cellular control mechanisms Cytokines Development and progression Disease Encephalomyelitis Encephalomyelitis, Autoimmune, Experimental - genetics Encephalomyelitis, Autoimmune, Experimental - immunology Experimental allergic encephalomyelitis FOXO1 protein Gene expression Genetic aspects Health aspects Helper cells Humans Inflammation Interleukin 17 Lymphocytes Lymphocytes T Mice Mice, Inbred C57BL MicroRNA MicroRNAs MicroRNAs - genetics miRNA Molecular modelling Multiple sclerosis Multiple Sclerosis - genetics Multiple Sclerosis - immunology Pathogenesis Patients T cells T-Lymphocytes, Regulatory Th1 Cells Th17 Cells Therapeutic targets Transcription factors |
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| Title | microRNA-92a promotes CNS autoimmunity by modulating the regulatory and inflammatory T cell balance |
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