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IL‐10 suppressor activity and ex vivo Tr1 cell function are impaired in multiple sclerosis

Acceso Cerrado
ID Minciencias: ART-0000268160-4
Ranking: ART-ART_A1

Abstract:

T regulatory cells type 1 (Tr1 cells) are excellent candidates for cell therapy in multiple sclerosis (MS). The aim of our study was to assess the functional state of Tr1 cells and IL-10R signaling in patients with MS. Tr1 cells were induced in vitro by activation with anti-CD46 antibodies in controls and patients with MS. Cells were phenotyped by cytometry and suppression assays, and the expression of cytokines and transcription factors was evaluated by real-time PCR, ELISA, cytometry and Western blotting. We found that the activity of Tr1 cells and IL-10R signaling is impaired in MS patients since Tr1 cells isolated from MS patients produced less IL-10 than those obtained from controls. Indeed, the supernatants from Tr1 cells from controls did not suppress the proliferation of stimulated CD4(+) cells from patients with MS. Furthermore, the IL-10R signaling pathway was not fully active in CD4(+) cells from MS patients and these cells had higher baseline levels of SOCS3 transcripts than controls. Indeed, after in vitro IL-10 stimulation, the expression levels of the STAT1, STAT3 and IL-10RA genes were higher in MS patients than in controls. Moreover, Stat-3 phosphorylation was lower in controls than in patients after IL-10 stimulation. These results indicate that IL-10 regulatory function is impaired in patients with MS.

Tópico:

Immunotherapy and Immune Responses

Citaciones:

Citations: 130
130

Citaciones por año:

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Paperbuzz Score: 0
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Información de la Fuente:

SCImago Journal & Country Rank
FuenteEuropean Journal of Immunology
Cuartil año de publicaciónNo disponible
Volumen38
Issue2
Páginas576 - 586
pISSNNo disponible
ISSN1521-4141

Enlaces e Identificadores:

Minciencias IDART-0000268160-4Scienti ID0000268160-4Openalex URLhttps://openalex.org/W2043149094
Doi URLhttps://doi.org/10.1002/eji.200737271Pmid URLhttps://pubmed.ncbi.nlm.nih.gov/18200504
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