Titolo | Role of regulatory t cells in rheumatoid arthritis: Facts and hypothesis |
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Tipo di pubblicazione | Articolo su Rivista peer-reviewed |
Anno di Pubblicazione | 2010 |
Autori | Alunno, Alessia, Bartoloni Elena, Nocentini Giuseppe, Bistoni Onelia, Ronchetti Simona, Petrillo Maria Grazia, Riccardi Carlo, and Gerli Roberto |
Rivista | Autoimmunity Highlights |
Volume | 1 |
Paginazione | 45 – 51 |
Type of Article | Review |
ISSN | 20383274 |
Parole chiave | adalimumab, biological marker, CD4+ CD25+ T lymphocyte, Cell expansion, cell function, Cell Surface, corticosteroid, cytokine response, cytotoxic T lymphocyte antigen 4, disease predisposition, drug effect, drug mechanism, glucocorticoid induced tumor necrosis factor receptor, human, immune dysregulation, immunological tolerance, Immunomodulation, immunopathogenesis, immunoregulation, infliximab, interleukin 6, nonhuman, Phenotype, priority journal, protein function, regulatory T lymphocyte, review, rheumatoid arthritis, T cell depletion, T lymphocyte activation, T lymphocyte subpopulation, tocilizumab, transcription factor FOXP3, transforming growth factor beta, tumor necrosis factor alpha, tumor necrosis factor inhibitor |
Abstract | Regulatory T cells (Treg) are a CD4+ lymphocyte subset involved in self-tolerance and autoimmunity prevention. There is evidence for a phenotypic and/or functional impairment of this cell subset during the natural history of several chronic autoimmune/inflammatory diseases, including rheumatoid arthritis (RA). Although the intracellular transcription factor FoxP3 is thought to be the master regulator of Treg cell function, a number of other molecules expressed on the cell surface have been proposed for the identification of Treg cells. This is important in order to favour their possible selective isolation and in the development of new therapeutic strategies. In the present paper, available data on phenotypic and functional characterization of Treg cells in both peripheral blood and synovial fluid from RA patients are reviewed and their possible pathogenic role in triggering and perpetuating rheumatoid joint inflammation is discussed. © Springer-Verlag 2010. |
Note | Cited by: 15; All Open Access, Bronze Open Access, Green Open Access |
URL | https://www.scopus.com/inward/record.uri?eid=2-s2.0-78249243246&doi=10.1007%2fs13317-010-0008-2&partnerID=40&md5=3b4dc7b08c815008f85b49e6827a3776 |
DOI | 10.1007/s13317-010-0008-2 |
Citation Key | Alunno201045 |