دورية أكاديمية
أعرض في EDS

Stem cell-derived tissue-associated regulatory T cells ameliorate the development of autoimmunity.

التفاصيل البيبلوغرافية
العنوان: Stem cell-derived tissue-associated regulatory T cells ameliorate the development of autoimmunity.
المؤلفون: Haque M; Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA., Song J; Institutes of Irradiation/Immunology, The Third Military Medical University, Chongqing 400038, China., Fino K; Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA., Sandhu P; Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA., Song X; Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA., Lei F; Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA., Zheng S; Department of Medicine, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA., Ni B; Institutes of Irradiation/Immunology, The Third Military Medical University, Chongqing 400038, China., Fang D; Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA., Song J; Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
المصدر: Scientific reports [Sci Rep] 2016 Feb 05; Vol. 6, pp. 20588. Date of Electronic Publication: 2016 Feb 05.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 101563288 Publication Model: Electronic Cited Medium: Internet ISSN: 2045-2322 (Electronic) Linking ISSN: 20452322 NLM ISO Abbreviation: Sci Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London : Nature Publishing Group, copyright 2011-
مواضيع طبية MeSH: Autoimmunity*, Adoptive Transfer/*methods , Arthritis, Experimental/*therapy , Induced Pluripotent Stem Cells/*cytology , T-Lymphocytes, Regulatory/*cytology, Animals ; Arthritis, Experimental/immunology ; Cell Line ; Cells, Cultured ; Coculture Techniques ; Disease Models, Animal ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Mice ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/metabolism ; T-Lymphocytes, Regulatory/immunology ; Transduction, Genetic
مستخلص: Pluripotent stem cells (PSCs) have the potential to produce almost all of the cells in the body, including regulatory T cells (Tregs). However, the exact conditions required for the development of antigen (Ag)-specific Tregs from PSCs (i.e., PSC-Tregs) are not well delineated. Ag-specific PSC-Tregs can be tissue/organ-associated and migrate to local inflamed tissues/organs to suppress the autoimmune response after adoptive transfer, thereby avoiding potential overall immunosuppression from non-specific Tregs. In this study, we developed a new approach to generate functional Ag-specific Tregs from induced PSCs (iPSCs), i.e., iPSC-Tregs, which had the ability to generate an Ag-specific immunosuppressive response in a murine model of arthritis. We retrovirally transduced murine iPSCs with a construct containing genes of Ag-specific T cell receptor (TCR) and the transcriptional factor FoxP3. We differentiated the iPSCs into Ag-specific iPSC-Tregs using in vitro or in vivo Notch signaling, and demonstrated that adoptive transfer of such Tregs dramatically suppressed autoimmunity in a well-established Ag-induced arthritis model, including the inflammation, joint destruction, cartilage prostaglandin depletion, osteoclast activity, and Th17 production. Our results indicate that PSCs can be used to develop Ag-specific Tregs, which have a therapeutic potential for Treg-based therapies of autoimmune disorders.
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معلومات مُعتمدة: R01 AI079056 United States AI NIAID NIH HHS; K18CA151798 United States CA NCI NIH HHS; R21AI109239 United States AI NIAID NIH HHS; R21 AI109239 United States AI NIAID NIH HHS; K18 CA151798 United States CA NCI NIH HHS
المشرفين على المادة: 0 (FOXP3 protein, human)
0 (Forkhead Transcription Factors)
0 (Receptors, Antigen, T-Cell)
تواريخ الأحداث: Date Created: 20160206 Date Completed: 20170104 Latest Revision: 20210102
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC4742827
DOI: 10.1038/srep20588
PMID: 26846186
قاعدة البيانات: MEDLINE
الوصف
تدمد:2045-2322
DOI:10.1038/srep20588