Interferon-β Modulates the Innate Immune Response against Glioblastoma Initiating Cells
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Interferon-β Modulates the Innate Immune Response against Glioblastoma Initiating Cells. / Wolpert, Fabian; Happold, Caroline; Reifenberger, Guido; Florea, Ana-Maria; Deenen, René; Roth, Patrick; Neidert, Marian Christoph; Lamszus, Katrin; Westphal, Manfred; Weller, Michael; Eisele, Günter.
in: PLOS ONE, Jahrgang 10, Nr. 10, 2015, S. e0139603.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Interferon-β Modulates the Innate Immune Response against Glioblastoma Initiating Cells
AU - Wolpert, Fabian
AU - Happold, Caroline
AU - Reifenberger, Guido
AU - Florea, Ana-Maria
AU - Deenen, René
AU - Roth, Patrick
AU - Neidert, Marian Christoph
AU - Lamszus, Katrin
AU - Westphal, Manfred
AU - Weller, Michael
AU - Eisele, Günter
PY - 2015
Y1 - 2015
N2 - Immunotherapy targeting glioblastoma initiating cells (GIC) is considered a promising strategy. However, GIC are prone to evade immune response and there is a need for potent adjuvants. IFN-β might enhance the immune response and here we define its net effect on the innate immunogenicity of GIC. The transcriptomes of GIC treated with IFN-β and controls were assessed by microarray-based expression profiling for altered expression of immune regulatory genes. Several genes involved in adaptive and innate immune responses were regulated by IFN-β. We validated these results using reverse transcription (RT)-PCR and flow cytometry for corresponding protein levels. The up-regulation of the NK cell inhibitory molecules HLA-E and MHC class I was balanced by immune stimulating effects including the up-regulation of nectin-2. In 3 out of 5 GIC lines tested we found a net immune stimulating effect of IFN-β in cytotoxicity assays using NKL cells as effectors. IFN-β therefore warrants further investigation as an adjuvant for immunotherapy targeting GIC.
AB - Immunotherapy targeting glioblastoma initiating cells (GIC) is considered a promising strategy. However, GIC are prone to evade immune response and there is a need for potent adjuvants. IFN-β might enhance the immune response and here we define its net effect on the innate immunogenicity of GIC. The transcriptomes of GIC treated with IFN-β and controls were assessed by microarray-based expression profiling for altered expression of immune regulatory genes. Several genes involved in adaptive and innate immune responses were regulated by IFN-β. We validated these results using reverse transcription (RT)-PCR and flow cytometry for corresponding protein levels. The up-regulation of the NK cell inhibitory molecules HLA-E and MHC class I was balanced by immune stimulating effects including the up-regulation of nectin-2. In 3 out of 5 GIC lines tested we found a net immune stimulating effect of IFN-β in cytotoxicity assays using NKL cells as effectors. IFN-β therefore warrants further investigation as an adjuvant for immunotherapy targeting GIC.
KW - Cell Adhesion Molecules
KW - Cell Line, Tumor
KW - Genes, MHC Class I
KW - Glioblastoma
KW - Histocompatibility Antigens Class I
KW - Humans
KW - Immunity, Innate
KW - Interferon-beta
KW - Nectins
KW - Up-Regulation
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.1371/journal.pone.0139603
DO - 10.1371/journal.pone.0139603
M3 - SCORING: Journal article
C2 - 26441059
VL - 10
SP - e0139603
JO - PLOS ONE
JF - PLOS ONE
SN - 1932-6203
IS - 10
ER -