ArticleBlood2018
MicroRNA-17-92 is required for T-cell and B-cell pathogenicity in chronic graft-versus-host disease in mice.
Article in Blood, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 63 citations in OpenAlex.
- 13q Deletion Syndrome Presenting with Lymphopenia Detected Through Newborn Screening for Primary Immunodeficiencies.International journal of molecular sciences · 2025Article
- Dimethyl fumarate ameliorates chronic graft-versus-host disease by inhibiting Tfh differentiation via Nrf2.Leukemia · 2025Article
- Monocytosis as prognostic factor for chronic graft versus host disease.Bone marrow transplantation · 2024Article
- Graft-Versus-Host Disease: Can Biomarkers Assist in Differential Diagnosis, Prognosis, and Therapeutic Strategy?Pharmaceuticals (Basel, Switzerland) · 2024Review
- Targeting PRMT1 prevents acute and chronic graft-versus-host disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Article
- MicroRNA profiling of low concentration extracellular vesicle RNA utilizing NanoString nCounter technology.Journal of extracellular biology · 2023Article
- Article
- The druggable transcription factor Fli-1 regulates T cell immunity and tolerance in graft-versus-host disease.The Journal of clinical investigation · 2022Article
- S1P/S1PR1 signaling differentially regulates the allogeneic response of CD4 and CD8 T cells by modulating mitochondrial fission.Cellular & molecular immunology · 2022Article
- Hypomethylation of miR-17-92 cluster in lupus T cells and no significant role for genetic factors in the lupus-associated DNA methylation signature.Annals of the rheumatic diseases · 2022Article
- MicroRNA serum profiles and chronic graft-versus-host disease.Blood advances · 2022Article
- Ceramide synthase 6 impacts T-cell allogeneic response and graft-versus-host disease through regulating N-RAS/ERK pathway.Leukemia · 2022Article
- MicroRNA-31 regulates T-cell metabolism via HIF1α and promotes chronic GVHD pathogenesis in mice.Blood advances · 2022Article
- The emerging role non-coding RNAs in B cell-related disorders.Cancer cell international · 2022Review
- Review
- Context-Dependent miR-21 Regulation of TLR7-Mediated Autoimmune and Foreign Antigen-Driven Antibody-Forming Cell and Germinal Center Responses.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- miR-20a suppresses Treg differentiation by targeting Map3k9 in experimental autoimmune encephalomyelitis.Journal of translational medicine · 2021Article
- Differentiation, functions, and roles of T follicular regulatory cells in autoimmune diseases.Inflammation and regeneration · 2021Review
- Noncoding RNAs in B cell responses.RNA biology · 2021Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Chronic graft-versus-host disease (cGVHD) is characterized as autoimmune-like fibrosis and antibody production mediated by pathogenic T cells and B cells. MicroRNA-17-92 (miR-17-92) influences the survival, differentiation, and function of lymphocytes in cancer, infections, and autoimmunity. To determine whether miR-17-92 regulates T- and B-cell responses in cGVHD, we generated mice conditionally deficient for miR-17-92 in T cells, B cells, or both. Using murine models of allogeneic bone marrow transplantation, we demonstrate that expression of miR-17-92 in donor T and B cells is essential for the induction of both scleroderma and bronchiolitis obliterans in cGVHD. Mechanistically, miR-17-92 expressed in T cells not only enhances the differentiation of pathogenic T helper 1 (Th1) and Th17 cells, but also promotes the generation of follicular Th cells, germinal center (GC) B cells, and plasma cells. In B cells, miR-17-92 expression is required for autoantibody production and immunoglobulin G deposition in the skin. Furthermore, we evaluated a translational approach using antagomirs specific for either miR-17 or miR-19, key members in miR-17-92 cluster. In a lupus-like cGVHD model, systemic administration of anti-miR-17, but not anti-miR-19, alleviates clinical manifestations and proteinuria incidence in recipients through inhibiting donor lymphocyte expansion, B-cell activation, and GC responses. Blockade of miR-17 also ameliorates skin damage by reducing Th17 differentiation in a scleroderma-cGVHD model. Taken together, our work reveals that miR-17-92 is required for T-cell and B-cell differentiation and function, and thus for the development of cGVHD. Furthermore, pharmacological inhibition of miR-17 represents a potential therapeutic strategy for the prevention of cGVHD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.