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J Cancer Res Clin Oncol ; 146(12): 3233-3240, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32865617

RESUMO

INTRODUCTION: The immunosuppressive tumor microenvironment promotes progression of pancreatic ductal adenocarcinoma (PDAC). γδ T cells infiltrate the pancreatic tumor stroma and support tumorigenesis through αß T cell inhibition. Pancreatic stellate cell (PSC) activation contributes to pancreatic fibrosis in PDAC, limiting the delivery and efficacy of therapeutic agents. Whether γδ T cells have direct effects on PSC activation is unknown. METHODS: In this study, we analyzed tumor tissue from 68 patients with PDAC and determined the frequency and location of γδ T cells using immunohistochemistry and immunofluorescence. PDAC samples from the TCGA database with low and high TRGC2 expression were correlated with the expression of extracellular matrix genes. Further, PSCs were isolated from pancreatic tumor tissue and co-cultured with γδ T cells for 48 hours and cytokine production was measured using a cytometric bead array. RESULTS: γδ T cells infiltrated the pancreatic tumor stroma and were located in proximity to PSCs. A high infiltration of γδ T cells was associated with increased expression of several extracellular matrix genes in human PDAC. In vitro, γδ T cells stimulated IL-6 production by PDAC-derived PSCs. CONCLUSION: γδ T cells activated PSCs and modulation of this interaction may enhance the efficacy of combinational therapies in human PDAC.


Assuntos
Adenocarcinoma/imunologia , Carcinoma Ductal Pancreático/imunologia , Interleucina-6/genética , Linfócitos Intraepiteliais/imunologia , Adenocarcinoma/genética , Adenocarcinoma/patologia , Carcinogênese/genética , Carcinogênese/imunologia , Carcinoma Ductal Pancreático/genética , Carcinoma Ductal Pancreático/patologia , Linhagem Celular Tumoral , Proliferação de Células , Técnicas de Cocultura , Matriz Extracelular/genética , Regulação Neoplásica da Expressão Gênica , Humanos , Células Estreladas do Pâncreas/imunologia , Células Estreladas do Pâncreas/metabolismo , Microambiente Tumoral/genética
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