Tumor-Derived Mesenchymal Stem Cells Use Distinct Mechanisms to Block the Activity of Natural Killer Cell Subsets.

Fiche du document

Auteurs
Date

19 septembre 2017

Type de document
Périmètre
Langue
Identifiant
Source

Serveur académique Lausannois

Relations

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.celrep.2017.08.089

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/28930684

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/2211-1247

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_7586A39849E65

Collection

Serveur Académique Lausannois

Organisation

Université de Lausanne et CHUV

Licences

info:eu-repo/semantics/openAccess , Copying allowed only for non-profit organizations , https://serval.unil.ch/disclaimer

Mots-clés 0

Aged; Aged, 80 and over; Carcinoma, Squamous Cell/pathology; Cell Separation; Coculture Techniques; Dinoprostone/metabolism; Down-Regulation; Female; Humans; Immunologic Factors/metabolism; Immunophenotyping; Immunosuppression; Interferon-gamma/metabolism; Interleukin-6/metabolism; Killer Cells, Natural/pathology; Lung Neoplasms/pathology; Lymphocytes, Tumor-Infiltrating/pathology; Male; Mesenchymal Stromal Cells/immunology; Mesenchymal Stromal Cells/metabolism; Middle Aged; Phenotype; Receptors, Immunologic/metabolism; Tumor Cells, Cultured; IL-6; PGE2; lung cancer; mesenchymal stem cells; natural killer cells

Sujets proches En

Carcinoma Cancers Malignancy (Cancer) Malignant tumors

Citer ce document

S. Galland et al., « Tumor-Derived Mesenchymal Stem Cells Use Distinct Mechanisms to Block the Activity of Natural Killer Cell Subsets. », Serveur académique Lausannois, ID : 10.1016/j.celrep.2017.08.089

Métriques

Partage / Export

Résumé 0

Mesenchymal stem cells (MSCs) display pleiotropic functions, which include secretion of soluble factors with immunosuppressive activity implicated in cancer progression. We compared the immunomodulatory effects on natural killer (NK) cells of paired intratumor (T)- and adjacent non-tumor tissue (N)-derived MSCs from patients with squamous cell lung carcinoma (SCC). We observed that T-MSCs were more strongly immunosuppressive than N-MSCs and affected both NK function and phenotype, as defined by CD56 expression. T-MSCs shifted NK cells toward the CD56 dim phenotype and differentially modulated CD56 bright/dim subset functions. Whereas MSCs affected both degranulation and activating receptor expression in the CD56 dim subset, they primarily inhibited interferon-γ production in the CD56 bright subset. Pharmacological inhibition of prostaglandin E2 (PGE2) synthesis and, in some MSCs, interleukin-6 (IL-6) activity restored NK function, whereas NK cell stimulation by PGE2 alone mimicked T-MSC-mediated immunosuppression. Our observations provide insight into how stromal responses to cancer dampen NK cell activity in human lung SCC.

document thumbnail

Par les mêmes auteurs

Sur les mêmes sujets

Exporter en