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Oxygen regulation of immunogenicity in primary human glioma cells

ABSTRACT: Dendritic Cell (DC) vaccination is a powerful approach for cancer immunotherapy that has recently obtained regulatory approval, and tumor lysate-pulsed DC vaccines are being tested in clinical trials. Tumor cell lysates (TLs) are often generated from cells cultured in atmospheric oxygen (~20% O2), which is roughly four-fold higher than that of the tumor in situ. We analyzed the expression patterns of glioma cells cultured in 5% Oxygen, 20% Oxygen and the primary tumors which the cell cultures were derived.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28316 | GEO | 2013/01/01

SECONDARY ACCESSION(S): PRJNA139333

REPOSITORIES: GEO

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Oxygen regulation of immunogenicity in primary human glioma cells

Project description:Dendritic Cell (DC) vaccination is a powerful approach for cancer immunotherapy that has recently obtained regulatory approval, and tumor lysate-pulsed DC vaccines are being tested in clinical trials. Tumor cell lysates (TLs) are often generated from cells cultured in atmospheric oxygen (~20% O2), which is roughly four-fold higher than that of the tumor in situ. We analyzed the expression patterns of glioma cells cultured in 5% Oxygen, 20% Oxygen and the primary tumors which the cell cultures were derived. Total RNA from primary resected glioma tumors or tumor cells cultured in in either 5% oxygen or 20% oxygen

2013-01-01 | E-GEOD-28316 | biostudies-arrayexpress

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Project description:The presence of high endothelial venules (HEV) and tertiary lymphoid structures (TLS) in solid tumors is correlated with favorable prognosis in many cancer types and has been associated with better treatment responses to immune-checkpoint blockade (ICB). However, the molecular mechanisms underlying intratumoral HEV and TLS formation and their contribution to anti-tumor responses remain unclear. Lymphotoxin beta receptor (LTBR) signaling is a critical regulator of lymph node organogenesis and when combined with antiangiogenic and ICB treatment can augment tumor-associated HEV formation. Here we demonstrate that LTBR signaling modulates the tumor microenvironment via multiple mechanisms to promote anti-tumor T cell responses. Systemic activation of the LTBR pathway via agonistic antibody treatment induced tumor-specific HEV formation, upregulated the expression of TLS-related chemokines, and enhanced dendritic cell (DC) and T cell infiltration and activation in syngeneic tumor models. In vitro studies confirmed direct effects of LTBR agonism on DC activation and maturation and associated DC- mediated T cell activation. Single agent LTBR agonist treatment inhibited syngeneic tumor growth in a CD8+ T cell- and HEV-dependent manner; and the LTBR agonist enhanced anti-tumor effects of anti-PD-1 and CAR T cell therapies, respectively. An in vivo tumor screen for TLS-inducing cytokines revealed that the combination of LTBR agonism and lymphotoxin alpha (LT⍺) expression promoted robust intratumoral TLS induction and enhanced tumor responses to anti-CTLA-4 treatment. Collectively, this study highlights crucial functions of LTBR signaling in modulating the tumor microenvironment and inform future HEV/TLS- based strategies for cancer treatments.

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Inhibition of p38 MAPK in DC progenitor cells endows DCs with superior immunogenicity

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