Kornelis S M van der Geest1, Katarzyna Smigielska-Czepiel2, Ji-Ah Park2, Wayel H Abdulahad2, Hye-Won Kim2, Bart-Jan Kroesen2, Anke van den Berg2, Annemieke M H Boots2, Eun-Bong Lee2, Elisabeth Brouwer2. 1. Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands, Division of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea, Department of Pathology and Medical Biology and Department of Laboratory Medicine, Section Medical Immunology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands, Division of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea, Department of Pathology and Medical Biology and Department of Laboratory Medicine, Section Medical Immunology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands k.s.m.van.der.geest@umcg.nl. 2. Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands, Division of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea, Department of Pathology and Medical Biology and Department of Laboratory Medicine, Section Medical Immunology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Abstract
OBJECTIVE: The aim of this study was to investigate the turnover of Treg cells in the SF of RA patients. METHODS: Treg cells were enumerated in peripheral blood and SF of RA patients and analysed by flow cytometry for expression of the proliferation marker Ki-67 and binding of the apoptosis marker annexin V. Sorted Treg cells of RA patients were analysed for expression of anti-apoptotic regulators Bcl-2 and microRNA-21 (miR-21) by RT-PCR. RESULTS: Treg cells displaying a memory phenotype were abundant in the SF of RA patients. SF Treg cells more frequently expressed the proliferation marker Ki-67 than conventional T cells. Only few SF Treg cells were apoptotic, as indicated by limited annexin V staining of these cells. SF Treg cells displayed high transcription levels of Bcl-2 and miR-21 in comparison with SF conventional T cells and peripheral blood Treg cells. CONCLUSION: Treg cells with a memory phenotype accumulate in the SF of RA patients. These Treg cells have a high proliferative activity and demonstrate little apoptosis. The latter finding could be explained by high transcription of Bcl-2 and miR-21 in SF Treg cells.
OBJECTIVE: The aim of this study was to investigate the turnover of Treg cells in the SF of RApatients. METHODS: Treg cells were enumerated in peripheral blood and SF of RApatients and analysed by flow cytometry for expression of the proliferation marker Ki-67 and binding of the apoptosis marker annexin V. Sorted Treg cells of RApatients were analysed for expression of anti-apoptotic regulators Bcl-2 and microRNA-21 (miR-21) by RT-PCR. RESULTS: Treg cells displaying a memory phenotype were abundant in the SF of RApatients. SF Treg cells more frequently expressed the proliferation marker Ki-67 than conventional T cells. Only few SF Treg cells were apoptotic, as indicated by limited annexin V staining of these cells. SF Treg cells displayed high transcription levels of Bcl-2 and miR-21 in comparison with SF conventional T cells and peripheral blood Treg cells. CONCLUSION: Treg cells with a memory phenotype accumulate in the SF of RApatients. These Treg cells have a high proliferative activity and demonstrate little apoptosis. The latter finding could be explained by high transcription of Bcl-2 and miR-21 in SF Treg cells.
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