Human articular chondrocytes regulate immune response by affecting directly T cell proliferation and indirectly inhibiting monocyte differentiation to professional antigen presenting cells.

Autologous Chondrocyte Implantation (ACI) 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. Allog...

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Main Authors: Rui Pereira, Daniela Martinelli, Ranieri Cancedda, Chiara Gentili, Alessandro Poggi
Format: Article
Language:English
Published: Frontiers Media S.A. 2016-10-01
Series:Frontiers in Immunology
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fimmu.2016.00415/full
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author Rui Pereira
Daniela Martinelli
Ranieri Cancedda
Chiara Gentili
Alessandro Poggi
author_facet Rui Pereira
Daniela Martinelli
Ranieri Cancedda
Chiara Gentili
Alessandro Poggi
author_sort Rui Pereira
collection DOAJ
description Autologous Chondrocyte Implantation (ACI) 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 (GM-CSF) and IL-4 (Mo) to professional antigen presenting cells (APC) such as dendritic cells (DC). Indeed, a marked inhibition of the onset of the CD1a expression and an ineffective down-regulation 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 alloresponse. The prostaglandin (PG) E2 present in the Mo-hAC co-culture conditioned media is a putative candidate of the hAC-mediated inhibition of Mo maturation. Altogether, these findings indicate that allogeneic hAC inhibit, rather than, trigger immune response and strongly suggest that an efficient chondrocyte implantation could be possible also in an allogeneic setting.
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spelling doaj.art-970478595d054c20aab38f1e9eb40dd72022-12-21T23:55:33ZengFrontiers Media S.A.Frontiers in Immunology1664-32242016-10-01710.3389/fimmu.2016.00415223439Human articular chondrocytes regulate immune response by affecting directly T cell proliferation and indirectly inhibiting monocyte differentiation to professional antigen presenting cells.Rui Pereira0Daniela Martinelli1Ranieri Cancedda2Chiara Gentili3Alessandro Poggi4University of GenovaUniversity of GenovaUniversity of GenovaUniversity of GenovaIRCCS AOU San Martino ISTAutologous Chondrocyte Implantation (ACI) 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 (GM-CSF) and IL-4 (Mo) to professional antigen presenting cells (APC) such as dendritic cells (DC). Indeed, a marked inhibition of the onset of the CD1a expression and an ineffective down-regulation 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 alloresponse. The prostaglandin (PG) E2 present in the Mo-hAC co-culture conditioned media is a putative candidate of the hAC-mediated inhibition of Mo maturation. Altogether, these findings indicate that allogeneic hAC inhibit, rather than, trigger immune response and strongly suggest that an efficient chondrocyte implantation could be possible also in an allogeneic setting.http://journal.frontiersin.org/Journal/10.3389/fimmu.2016.00415/fullimmune responseT lymphocyteDentritic cellsChondrocyte implantationAntigen presenting cells (APC)allogenic cells
spellingShingle Rui Pereira
Daniela Martinelli
Ranieri Cancedda
Chiara Gentili
Alessandro Poggi
Human articular chondrocytes regulate immune response by affecting directly T cell proliferation and indirectly inhibiting monocyte differentiation to professional antigen presenting cells.
Frontiers in Immunology
immune response
T lymphocyte
Dentritic cells
Chondrocyte implantation
Antigen presenting cells (APC)
allogenic cells
title Human articular chondrocytes regulate immune response by affecting directly T cell proliferation and indirectly inhibiting monocyte differentiation to professional antigen presenting cells.
title_full Human articular chondrocytes regulate immune response by affecting directly T cell proliferation and indirectly inhibiting monocyte differentiation to professional antigen presenting cells.
title_fullStr Human articular chondrocytes regulate immune response by affecting directly T cell proliferation and indirectly inhibiting monocyte differentiation to professional antigen presenting cells.
title_full_unstemmed Human articular chondrocytes regulate immune response by affecting directly T cell proliferation and indirectly inhibiting monocyte differentiation to professional antigen presenting cells.
title_short Human articular chondrocytes regulate immune response by affecting directly T cell proliferation and indirectly inhibiting monocyte differentiation to professional antigen presenting cells.
title_sort human articular chondrocytes regulate immune response by affecting directly t cell proliferation and indirectly inhibiting monocyte differentiation to professional antigen presenting cells
topic immune response
T lymphocyte
Dentritic cells
Chondrocyte implantation
Antigen presenting cells (APC)
allogenic cells
url http://journal.frontiersin.org/Journal/10.3389/fimmu.2016.00415/full
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