Tumor progression is associated with an immunosuppressive microenvironment that consists of several elements, such as regulatory T cells, type 2 macrophages and myeloid-derived suppressor cells. Here, we identify for the first time a BDCA1+CD14+ population of immunosuppressive cells that resides both in the blood and tumor of melanoma patients. We demonstrated that the presence of these cells in dendritic cell (DC)-based anti-tumor vaccines significantly suppresses CD4+ T cells in an antigen-specific manner. In an attempt to reveal the mechanism of this suppressive activity, we noticed that BDCA1+CD14+ cells express elevated levels of the check-point molecule PD-L1, which thereby hinders T cell proliferation. Importantly, although this suppressive BDCA1+CD14+ population expresses markers of both BDCA1+ DCs and monocytes, functional, transcriptome and proteome analyses clearly revealed that they comprise a unique population of cells that is exploited by tumors to evade immunity. Thus, targeting these cells may improve the efficacy of cancer immunotherapy.
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View SamplesWe purified five subsets representing the main stages of human precursor-B-cell differentiation and CD34+lin- cord blood cells. The immunoglobulin (Ig) gene rearrangement status was determined using TaqMan quantitative PCR and GeneScan analysis. To gain more insight in the networks of genes that initiate and/or regulate the different types of Ig gene rearrangements, we analyzed their gene expression profiles by correlating the initiation of Ig gene rearrangements with specific upregulation of transcription factors. In addition to previously described transcription factors, we identified 16 candidate genes involved in initiation and/or regulation of Ig gene rearrangements.
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Specimen part
View SamplesTo gain more insight into initiation and regulation of T cell receptor (TCR) gene rearrangement during human T cell development, we analyzed TCR gene rearrangements by quantitative PCR analysis in nine consecutive T-cell developmental stages, including CD34+ lin- cord blood cells as a reference. The same stages were used for gene expression profiling using DNA microarrays.
New insights on human T cell development by quantitative T cell receptor gene rearrangement studies and gene expression profiling.
Specimen part
View SamplesInvestigation of pH induced gene expression changes in bone-marrow-derived macrophages
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Sex, Age, Specimen part, Disease, Treatment
View SamplesInverstigation of differential gene expresseion in tumor-associated macrophages of WT-and Icer- knockout mice
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Sex, Age, Specimen part, Disease
View SamplesRNA-Seq analysis was used to study the profile of CD8 t cells from melanoma patients before and after treatment to detect transcriptional changes in peripheral blood
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Sex, Age, Specimen part, Disease
View SamplesHuman NK cells were sorted into CD56dim and CD56bright NK cell subpopulations. In order to define characteristics of both populations gene profiling was performed using Affymetrix arrays U133a and U133B.
Gene and protein characteristics reflect functional diversity of CD56dim and CD56bright NK cells.
Specimen part
View SamplesTo induce a differentiated phenotype, primary pancreatic TIC cultures were grown in 10% FBS containing conditions. To analyze gene expression changes upon induction of a differentiated phenotype, total RNA of cells cultured in FBS containing conditions and parallel control cells cultured under serum-free conditions was isolated and comparative gene expression profiling was performed.
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View SamplesComparatative gene expression analysis for CD4 T cell subsets isolated from peripheral blood and palatine tonsils
A methodology for global validation of microarray experiments.
Specimen part
View SamplesRituximab, a monoclonal antibody against CD20, has achieved great success in the treatment of B cell lymphoma, but many patients have shown resistance to it and led to disease progression eventually. At present, the mechanism of resistance is still not clear, but we consider that it may involve the multiple genes and multiple signaling pathways. Therefore, our study aimed at searching differentially expressed genes of rituximab resistant cell lines (RRCL) by cDNA microarray, and exploring the resistant mechanism of RRCL by using the subsequent bioinformatics methods. In this study, we successfully identified seventy up-regulated genes and forty-two down-regulated genes in both two RRCL. We also isolated the MAPK signaling pathway, which was the significantly enriched pathway in resistant mechanism, through KEGG pathway analysis. Moreover, we discovered the biological behaviors of RRCL that mainly inhibit apoptosis, promote cellular proliferation, transcription and angiogenesis through Gene Ontology (GO) terms analysis. In conclusion, our results suggested that the most closely related pathway to rituximab resistance was MAPK signaling pathway, which may partly be related to its inhibiting the apoptosis of cells and promoting the proliferation of cells and vascular development.
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Specimen part, Cell line
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