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Article: Human Articular Chondrocytes Regulate Immune Response by Affecting Directly T Cell Proliferation and Indirectly Inhibiting Monocyte Differentiation to Professional Antigen-Presenting Cells.

Pereira, Rui C / Martinelli, Daniela / Cancedda, Ranieri / Gentili, Chiara / Poggi, Alessandro

Frontiers in immunology

2016  Volume 7, Page(s) 415

Abstract: ... with granulocyte monocyte colony-stimulating factor and IL-4 (Mo) to professional antigen-presenting cells ... of the autologous chondrocytes and a satisfactory outcome of the implant. Allogeneic human articular chondrocytes ... to antigen-dependent and -independent proliferative stimuli. This effect was maximal when T cells and hAC ...

Abstract Autologous chondrocyte implantation is the current gold standard cell therapy for cartilage lesions. However, in some instances, the heavily compromised health of the patient can either impair or limit the recovery of the autologous chondrocytes and a satisfactory outcome of the implant. Allogeneic human articular chondrocytes (hAC) could be a good alternative, but the possible immunological incompatibility between recipient and hAC donor should be considered. Herein, we report that allogeneic hAC inhibited T lymphocyte response to antigen-dependent and -independent proliferative stimuli. This effect was maximal when T cells and hAC were in contact and it was not relieved by the addition of exogenous lymphocyte growth factor interleukin (IL)-2. More important, hAC impaired the differentiation of peripheral blood monocytes induced with granulocyte monocyte colony-stimulating factor and IL-4 (Mo) to professional antigen-presenting cells, such as dendritic cells (DC). Indeed, a marked inhibition of the onset of the CD1a expression and an ineffective downregulation of CD14 antigens was observed in Mo-hAC co-cultures. Furthermore, compared to immature or mature DC, Mo from Mo-hAC co-cultures did not trigger an efficacious allo-response. The prostaglandin (PG) E
Language English
Publishing date 2016
Publishing country Switzerland
Document type Journal Article
ZDB-ID 2606827-8
ISSN 1664-3224
ISSN 1664-3224
DOI 10.3389/fimmu.2016.00415
Database MEDical Literature Analysis and Retrieval System OnLINE

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