학술논문
Characterization of the MT-2 Treg-like cell line in the presence and absence of forkhead box P3 (FOXP3).
Document Type
Academic Journal
Author
McCullough MJ; Division of Pulmonary Diseases and Critical Care Medicine, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA.; Marsico Lung Institute, University of North Carolina, Chapel Hill, NC, USA.; Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC, USA.; Tune MK; Division of Pulmonary Diseases and Critical Care Medicine, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA.; Marsico Lung Institute, University of North Carolina, Chapel Hill, NC, USA.; Cabrera JC; Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.; Torres-Castillo J; Division of Pulmonary Diseases and Critical Care Medicine, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA.; Marsico Lung Institute, University of North Carolina, Chapel Hill, NC, USA.; He M; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.; Feng Y; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.; Doerschuk CM; Division of Pulmonary Diseases and Critical Care Medicine, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA.; Marsico Lung Institute, University of North Carolina, Chapel Hill, NC, USA.; Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC, USA.; Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.; Center for Airways Disease, University of North Carolina, Chapel Hill, NC, USA.; Dang H; Marsico Lung Institute, University of North Carolina, Chapel Hill, NC, USA.; Beltran AS; Department of Genetics, School of Medicine, University of North Carolina, Chapel Hill, NC, USA.; Hagan RS; Division of Pulmonary Diseases and Critical Care Medicine, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA.; Marsico Lung Institute, University of North Carolina, Chapel Hill, NC, USA.; Mock JR; Division of Pulmonary Diseases and Critical Care Medicine, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA.; Marsico Lung Institute, University of North Carolina, Chapel Hill, NC, USA.; Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC, USA.
Source
Publisher: Wiley Country of Publication: United States NLM ID: 8706300 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1440-1711 (Electronic) Linking ISSN: 08189641 NLM ISO Abbreviation: Immunol Cell Biol Subsets: MEDLINE
Subject
Language
English
Abstract
CD4 + forkhead box P3 (FOXP3) + regulatory T cells (Tregs) are essential in maintaining immune tolerance and suppressing excessive immune responses. Tregs also contribute to tissue repair processes distinct from their roles in immune suppression. For these reasons, Tregs are candidates for targeted therapies for inflammatory and autoimmune diseases, and in diseases where tissue damage occurs. MT-2 cells, an immortalized Treg-like cell line, offer a model to study Treg biology and their therapeutic potential. In the present study, we use clustered regularly interspaced palindromic repeats (CRISPR)-mediated knockdown of FOXP3 in MT-2 cells to understand the transcriptional and functional changes that occur when FOXP3 is lost and to compare MT-2 cells with primary human Tregs. We demonstrate that loss of FOXP3 affects the transcriptome of MT-2 cells and that FOXP3's potential downstream targets include a wide range of transcripts that participate in the cell cycle, promote growth and contribute to inflammatory processes, but do not wholly simulate previously reported human primary Treg transcriptional changes in the absence of FOXP3. We also demonstrate that FOXP3 regulates cell cycling and proliferation, expression of molecules crucial to Treg function and MT-2 cell-suppressive activities. Thus, MT-2 cells offer opportunities to address regulatory T-cell functions in vitro.
(© 2024 the Australian and New Zealand Society for Immunology, Inc.)
(© 2024 the Australian and New Zealand Society for Immunology, Inc.)