Malignant glioma cells counteract antitumor immune responses through expression of lectin-like transcript-1

Patrick Roth; Michel Mittelbronn; Wolfgang Wick; Richard Meyermann; Marcos Tatagiba; Michael Weller

doi:10.1158/0008-5472.CAN-06-4783

Malignant glioma cells counteract antitumor immune responses through expression of lectin-like transcript-1

Patrick Roth^*, Michel Mittelbronn, Wolfgang Wick, Richard Meyermann, Marcos Tatagiba, Michael Weller

^*Corresponding author for this work

Research output: Contribution to journal › Article › Research › peer-review

87 Citations (Scopus)

Abstract

Glioblastoma, one of the most lethal tumors, is paradigmatic for tumor-associated immunosuppression. Lectin-like transcript-1 (LLT1) is a newly identified ligand for the inhibitory natural killer (NK) cell receptor CD161. Here, we report that glioma cells express LLT1 mRNA and protein in vitro and in vivo, whereas expression levels in normal brain are low. LLT1 expression in human gliomas increases with the WHO grade of malignancy. We further show that transforming growth factor-β (TGF-β) up-regulates the expression of LLT1 in glioma cells. Small interfering RNA (siRNA)-mediated down-regulation of LLT1 in LNT-229 and LN-428 cells promotes their lysis by NK cells. Thus, LLT1 acts as a mediator of immune escape and contributes to the immunosuppressive properties of glioma cells.

Original language	English
Pages (from-to)	3540-3544
Number of pages	5
Journal	Cancer Research
Volume	67
Issue number	8
DOIs	https://doi.org/10.1158/0008-5472.CAN-06-4783
Publication status	Published - 15 Apr 2007
Externally published	Yes

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title = "Malignant glioma cells counteract antitumor immune responses through expression of lectin-like transcript-1",

abstract = "Glioblastoma, one of the most lethal tumors, is paradigmatic for tumor-associated immunosuppression. Lectin-like transcript-1 (LLT1) is a newly identified ligand for the inhibitory natural killer (NK) cell receptor CD161. Here, we report that glioma cells express LLT1 mRNA and protein in vitro and in vivo, whereas expression levels in normal brain are low. LLT1 expression in human gliomas increases with the WHO grade of malignancy. We further show that transforming growth factor-β (TGF-β) up-regulates the expression of LLT1 in glioma cells. Small interfering RNA (siRNA)-mediated down-regulation of LLT1 in LNT-229 and LN-428 cells promotes their lysis by NK cells. Thus, LLT1 acts as a mediator of immune escape and contributes to the immunosuppressive properties of glioma cells.",

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T1 - Malignant glioma cells counteract antitumor immune responses through expression of lectin-like transcript-1

AU - Roth, Patrick

AU - Mittelbronn, Michel

AU - Wick, Wolfgang

AU - Meyermann, Richard

AU - Tatagiba, Marcos

AU - Weller, Michael

PY - 2007/4/15

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N2 - Glioblastoma, one of the most lethal tumors, is paradigmatic for tumor-associated immunosuppression. Lectin-like transcript-1 (LLT1) is a newly identified ligand for the inhibitory natural killer (NK) cell receptor CD161. Here, we report that glioma cells express LLT1 mRNA and protein in vitro and in vivo, whereas expression levels in normal brain are low. LLT1 expression in human gliomas increases with the WHO grade of malignancy. We further show that transforming growth factor-β (TGF-β) up-regulates the expression of LLT1 in glioma cells. Small interfering RNA (siRNA)-mediated down-regulation of LLT1 in LNT-229 and LN-428 cells promotes their lysis by NK cells. Thus, LLT1 acts as a mediator of immune escape and contributes to the immunosuppressive properties of glioma cells.

AB - Glioblastoma, one of the most lethal tumors, is paradigmatic for tumor-associated immunosuppression. Lectin-like transcript-1 (LLT1) is a newly identified ligand for the inhibitory natural killer (NK) cell receptor CD161. Here, we report that glioma cells express LLT1 mRNA and protein in vitro and in vivo, whereas expression levels in normal brain are low. LLT1 expression in human gliomas increases with the WHO grade of malignancy. We further show that transforming growth factor-β (TGF-β) up-regulates the expression of LLT1 in glioma cells. Small interfering RNA (siRNA)-mediated down-regulation of LLT1 in LNT-229 and LN-428 cells promotes their lysis by NK cells. Thus, LLT1 acts as a mediator of immune escape and contributes to the immunosuppressive properties of glioma cells.

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Malignant glioma cells counteract antitumor immune responses through expression of lectin-like transcript-1

Abstract

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