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.
Tissue Cell ; 63: 101320, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32223948

RESUMO

Multipotent mesenchymal stromal cells (MSCs) are characterized by immunomodulatory properties along with the high proliferative and paracrine activity, as well as multilineage potency. The effects of MSCs on the T cell adaptive immunity are of a special interest. Low O2 level (1-7 %) is known to be typical for the putative site of the MSC - T cell interactions. A comparative evaluation of the effects of adipose tissue derived MSC (ASCs) on the mitogen-stimulated T cells at the ambient (20 %) and tissue-related (5 %) O2 levels demonstrated reduced T cell activation by the HLA-DR expression, decreased pro-inflammatory and increased anti-inflammatory cytokine production in co-culture, inhibited T cell proliferation, with the effects increased at hypoxia. T cell interactions with ASCs resulted in the up-regulation of PDCD1, Foxp3, and TGFß1 known to play an important role in the immune response suppression, and in the down-regulation of genes involved in the inflammatory reaction (IL2, IFNG). These changes were significantly increased under hypoxia. At the same time, neither ASCs nor the reduced O2 level had negative effects on the viability of T cells.


Assuntos
Imunidade Adaptativa/genética , Células-Tronco Mesenquimais/metabolismo , Oxigênio/metabolismo , Linfócitos T/imunologia , Imunidade Adaptativa/imunologia , Adipócitos/imunologia , Adipócitos/metabolismo , Tecido Adiposo/imunologia , Tecido Adiposo/metabolismo , Comunicação Celular/genética , Hipóxia Celular/genética , Proliferação de Células/genética , Fatores de Transcrição Forkhead/genética , Regulação da Expressão Gênica/genética , Antígenos HLA-DR/genética , Humanos , Interferon gama/genética , Interleucina-2/genética , Células-Tronco Mesenquimais/imunologia , Células-Tronco Mesenquimais/patologia , Oxigênio/imunologia , Comunicação Parácrina/genética , Receptor de Morte Celular Programada 1/genética , Linfócitos T/metabolismo , Fator de Crescimento Transformador beta1/genética
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA