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Human articular chondrocytes suppress in vitro proliferation of anti-CD3 activated peripheral blood mononuclear cells

✍ Scribed by Chiara Bocelli-Tyndall; Andrea Barbero; Christian Candrian; Rhodri Ceredig; Alan Tyndall; Ivan Martin


Publisher
John Wiley and Sons
Year
2006
Tongue
English
Weight
153 KB
Volume
209
Category
Article
ISSN
0021-9541

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✦ Synopsis


Abstract

Objective: To investigate whether mature human articular chondrocytes (AC) exhibit an antiproliferative effect on activated peripheral blood mononuclear cells (PBMC) and to compare this effect with other cells of mesenchymal origin. Methods: AC from healthy cadaveric cartilage were grown for different passages, in the absence (control) or presence of factors enhancing cell de‐differentiation (transforming growth factor (TGF)β1, fibroblast growth factor (FGF)‐2, and platelet derived growth factor (PDGF)bb‐TFP medium). Cell ability to suppress PBMC proliferation driven by anti‐CD3 antibody was measured by tritiated thymidine uptake following incubation for 48 h at different PBMC:AC ratios and expressed as percent of residual proliferation (RP). AC antiproliferative effect was compared to that of control dermal fibroblasts (DF) and bone marrow stromal cells (BMSC). Results: AC exhibited a cell number‐dependent antiproliferative effect. The strongest effect (up to 2% RP) was measured using the least expanded AC cultures. The use of TFP medium for AC expansion resulted in a significantly lower antiproliferative effect, in the range of that induced by BMSC (up to 18% RP). Also DF induced a marked antiproliferative effect (up to 11% RP). Conclusion: We report for the first time that human AC have a marked antiproliferative effect on anti‐CD3 stimulated PBMC, which is reduced upon culture in medium‐inducing extensive cell de‐differentiation. These results reflect the immunosuppressive properties observed for other different mesenchymal cell types and raise the question of a potential common physiological role in local tissue protection. J. Cell. Physiol. 209: 732–734, 2006. © 2006 Wiley‐Liss, Inc.


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