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Anti-CD3 Antibody Induces IL-10-producing CD4+CD25+ Regulatory T Cells, Which Suppress T Cell Response in Rheumatoid Arthritis Patients
Immune Network ; : 124-132, 2007.
Article em En | WPRIM | ID: wpr-195141
Biblioteca responsável: WPRO
ABSTRACT
BACKGROUND: Regulatory T cells (Tregs) have been investigated intensively for some decades. These cells regulate the immune system, prevent overactivated immune responses and can be used therapeutically. For rheumatoid arthritis (RA), understanding the functions and status of Tregs is an important step for understanding immune regulation in this autoimmune disease. METHODS: We investigated the percentages, phenotypes and suppressive functions of CD4+CD25+ Tregs in peripheral blood (PB) of patients with RA. RESULTS: The percentages were higher in the patients (n=12) than in healthy controls (n=10), and the cells expressed the CD45RBlow, CTLA-4 and CCR7 phenotypes. We also investigated the expression of Foxp3 and secretion of interleukin (IL)-10 induced CD4+CD25+ Tcells by anti-CD3 antibody treatment. A suppressive function of the patients' cells was shown through coculture with CD4+CD25+ T cells in vitro. CONCLUSION: We suggest that, despite their increased numbers and suppressive function, they manage the ongoing inflammation ineffectively. It might be possible to apply IL-10 to induce the proliferation of IL-10-producing Tregs as therapy for RA.
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Texto completo: 1 Índice: WPRIM Assunto principal: Fenótipo / Artrite Reumatoide / Doenças Autoimunes / Linfócitos T / Interleucinas / Interleucina-10 / Linfócitos T Reguladores / Técnicas de Cocultura / Sistema Imunitário / Inflamação Limite: Humans Idioma: En Revista: Immune Network Ano de publicação: 2007 Tipo de documento: Article
Texto completo: 1 Índice: WPRIM Assunto principal: Fenótipo / Artrite Reumatoide / Doenças Autoimunes / Linfócitos T / Interleucinas / Interleucina-10 / Linfócitos T Reguladores / Técnicas de Cocultura / Sistema Imunitário / Inflamação Limite: Humans Idioma: En Revista: Immune Network Ano de publicação: 2007 Tipo de documento: Article