Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Cell Immunol ; 310: 108-115, 2016 12.
Artigo em Inglês | MEDLINE | ID: mdl-27576175

RESUMO

Mesenchymal stem cells (MSCs) have strong immunomodulatory properties, however these properties may show some differences according to the tissue type of their isolate. In this study we investigated the paracrine interactions between human DP derived MSCs (hDP-MSCs) and the CD4+ T helper cell subsets to establish their immunomodulatory mechanisms. We found that the CD4+-Tbet+ (Th1) and CD4+-Gata3+ (Th2) cells were suppressed by the hDP-MSCs, but the CD4+-Stat3+ (Th17) and CD4+-CD25+-FoxP3+ (Treg) cells were stimulated. The expressions of T cell specific cytokines interferon gamma (IFN-g), interleukin (IL)-4 and IL-17a decreased, but IL-10 and transforming growth factor beta-1 (TGF-b1) increased with the hDP-MSCs. The expressions of indoleamine-pyrrole 2,3-dioxygenase (IDO), prostaglandin E2 (PGE2), soluble human leukocyte antigen G (sHLA-G) derived from hDP-MSCs slightly increased, but hepatocyte growth factor (HGF) significantly increased in the co-culture groups. According to our findings, the hDP-MSCs can suppress the Th1 and Th2 subsets but stimulate the Th17 and Treg subsets. The Stat3 expression of Th17 cells may have been stimulated by the HGF, and thus the pro-inflammatory Th17 cells may have altered into the immunosuppressive regulatory Th17 cells. Further prospective studies are needed to confirm our findings.


Assuntos
Células-Tronco Mesenquimais/fisiologia , Linfócitos T Reguladores/imunologia , Células Th1/imunologia , Células Th17/imunologia , Células Th2/imunologia , Diferenciação Celular , Células Cultivadas , Polpa Dentária/patologia , Dinoprostona/metabolismo , Fatores de Transcrição Forkhead/metabolismo , Fator de Transcrição GATA3/metabolismo , Fator de Crescimento de Hepatócito/metabolismo , Humanos , Imunomodulação , Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo , Comunicação Parácrina , Fator de Transcrição STAT3/metabolismo , Proteínas com Domínio T/metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA