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2016 ; 7
(ä): 415
Nephropedia Template TP
gab.com Text
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English Wikipedia
Human Articular Chondrocytes Regulate Immune Response by Affecting Directly T
Cell Proliferation and Indirectly Inhibiting Monocyte Differentiation to
Professional Antigen-Presenting Cells
#MMPMID27822208
Pereira RC
; Martinelli D
; Cancedda R
; Gentili C
; Poggi A
Front Immunol
2016[]; 7
(ä): 415
PMID27822208
show ga
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(2) 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.