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Differential gene expression of T-cell lymphomas (TCL) upon engagement of T-cell receptor (TCR) signaling [TCL1; T8ML1]

ABSTRACT: To study differential gene expression of TCLs upon TCR signaling, three TCL primary cells and one TCL cell line T8ML1 were chosen for this study. The prmiary TCL cells consist of TCL1 and TCL2 (sezary patients) and TCL3 (PTCL, NOS patient). The TCR signaling was engaged by anti-CD3/CD28 treatment in vitro. The TCL cells were treated without/with anti-CD3/CD28 for different time periods in vitro in cell culture. The total RNA was isolated from the TCLs and subjected to affimetry microarray (GPL17692) analysis. The differential gene expression of individual TCL was identified as well as a set of common genes invloved in TCR signaling in TCLs. The subject for this study includes pirmary cells isolated from three TCL patients [two sezary patients (TCL1 & TCL2) and one PTCL, NOS patient (TCL3)] and cells from a TCL cell line (T8ML1). The purity of isolated primary cells is >93% as idnetified by flow cytometry. The TCLs were treated with/without anti-CD3/CD28 for different time points, with 2-3 replicates for each time point. Gene expression value was presented as Log2 transformed. Differntial expressed genes were identified by ∆log2x>1 in comparison to no anti-CD3/CD28 treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE77875 | GEO | 2017/02/10

SECONDARY ACCESSION(S): PRJNA311941

REPOSITORIES: GEO

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Differential gene expression of T-cell lymphomas (TCL) upon engagement of T-cell receptor (TCR) signaling [TCL3]

Project description:To study differential gene expression of TCLs upon TCR signaling, three TCL primary cells and one TCL cell line T8ML1 were chosen for this study. The prmiary TCL cells consist of TCL1 and TCL2 (sezary patients) and TCL3 (PTCL, NOS patient). The TCR signaling was engaged by anti-CD3/CD28 treatment in vitro. The TCL cells were treated without/with anti-CD3/CD28 for different time periods in vitro in cell culture. The total RNA was isolated from the TCLs and subjected to affimetry microarray (GPL17692) analysis. The differential gene expression of individual TCL was identified as well as a set of common genes invloved in TCR signaling in TCLs.

2017-02-10 | GSE77877 | GEO

Differential gene expression of T-cell lymphomas (TCL) upon engagement of T-cell receptor (TCR) signaling [TCL2]

2017-02-10 | GSE77876 | GEO

DNMT3A mutations define a unique biological and prognostic subgroup associated with cytotoxic T-cells in PTCL-NOS [RNA-Seq]

Project description:Peripheral T-cell lymphomas (PTCLs) are heterogenous T-cell neoplasms often associated with epigenetic dysregulation. We investigated de novo DNA methyltransferase 3A (DNMT3A) mutations in common PTCL entities, including angioimmunoblastic T-cell lymphoma and novel molecular subtypes identified within PTCL-not otherwise specified (PTCL-NOS) designated as PTCL-GATA3 and PTCL-TBX21. DNMT3A-mutated PTCL-TBX21 cases showed inferior overall-survival, with DNMT3A mutated residues skewed towards the methyltransferase domain and dimerization motif (S881–R887). Transcriptional profiling demonstrated significant enrichment of activated CD8+ T-cell cytotoxic gene signatures in the DNMT3A-mutant PTCL-TBX21 cases, which was further validated using immunohistochemistry. Genome-wide methylation analysis of DNMT3A-mutant versus wild-type PTCL-TBX21 cases demonstrated hypomethylation in target genes regulating IFN-g, TCR signaling and EOMES, a master transcriptional regulator of cytotoxic effector cells. Similar findings were observed in a murine model of PTCL with Dnmt3a loss (in-vivo) and further validated in-vitro by ectopic expression of DNMT3A-mutants (DNMT3A-R882, -Q886, -V716, versus WT) in CD8+T-cell line, resulting in T-cell activation and EOMES upregulation. Furthermore, stable, ectopic expression of the DNMT3A-mutants in primary CD3+ T-cell cultures resulted in the preferential outgrowth of CD8+ T-cells with DNMT3AR882H mutation. Single-cell-RNA-seq analysis of CD3+ T-cells revealed differential CD8+ T-cell subset polarization, mirroring findings in DNMT3A-mutated PTCL-TBX21 and validating the cytotoxic and T-cell memory transcriptional programs associated with the DNMT3AR882H mutation. Our findings indicate that DNMT3A mutations define a cytotoxic subset in PTCL-TBX21 with prognostic significance, thus may further refine pathological heterogeneity in PTCL-NOS and suggest alternative treatment strategies for this subset.

2022-05-29 | GSE204876 | GEO

DNMT3A mutations define a unique biological and prognostic subgroup associated with cytotoxic T-cells in PTCL-NOS [meDIP-Seq]

2022-05-29 | GSE204875 | GEO

RNA-seq profiling of in vitro FRC-conditioned, IL6-conditioned or control (anti-CD3/CD28)-stimulated CD8+ T cells

Project description:To broadly assess which pathways FRCs regulate in CD8+ T cells, we sorted CD8+ T cells for RNA-seq following activation in whole splenocyte mixtures via soluble anti-CD3/CD28 for 48 hours (Stim), activated with anti-CD3/CD28 in the presence of Nos2–/– FRCs (FRC) or activated with anti-CD3/CD28 plus 100 ng/ml recombinant IL-6 (IL-6). Here we demonstrate that FRC-derived signals, including IL-6, act in concert with TCR signaling and co-stimulation to promote the expression of MYC and HIF-1-dependent glycolytic genes and vital pro-survival genes (encoding BCL-2 family members, inhibitors of apoptosis [IAPs] members and Cflar) in activated CD8+ T cells.

2019-10-14 | GSE136898 | GEO

SNP array genomic profiling of PTCL NOS

Project description:DNA extracted from frozen tissue of 47 peripheral T-cell lymphomasânot otherwise specified [PTCL-NOS] was hybridized to 250k StyI SNP arrays 47 PTCL NOS compared to healthy reference DNA. DNA of PTCL NOS was extracted from frozen tissue blocks, DNA of healthy individual was extracted from peripheral blood mononuclear cells. Array hybridization was performed according to manufacturerÂ´s protocol.

2010-03-17 | E-GEOD-15842 | biostudies-arrayexpress

Microarray analysis of WT and Tfap4-KO CD8 T cells during early activation

Project description:Gene expression of Tfap4â/â and WT CD8+ T cells were compared after activation with anti-CD3 and anti-CD28 antibodies in vitro or with Listeria monocytogenes infection in vivo For in vitro activation, naive CD8+ T cells were purified from WT and Tfap4â/â mice and activated with anti-CD3 and anti-CD28 antibodies for 72 hours. For in vivo activation, naive CD8+ T cells from Tfap4â/â OT-I or control WT OT-I TCR transgenice mice were adoptively transferred to congenic host mice that were subsequently infected with Listeria mnocytogenes expression ovalbumin. Activated OT-I cells were harvested 48 hours after infection.

2014-07-13 | E-GEOD-58078 | biostudies-arrayexpress

Gene expression in CD8+ T cells derived from Nrdp1+/+ and Nrdp1-/- mice

Project description:The purpose of this study was to determine which genes are differentially regulated by the E3 ligase Nrdp1 in CD8+ T cells after treatments with anti-CD3/CD28 Abs. The results demonstrate increased induction of cytotoxicity-associated genes in Nrdp1-/- mice than in Nrdp1+/+ mice after activation. Thus Nrdp1 may be involved in the regulation of TCR signaling. Naive CD8+ T cells derived spleens of Nrdp1+/+ and Nrdp1-/- mice were either untreated or treated with immobilized anti-CD3 (5 μg/ml) and soluble anti-CD28 (1 μg/ml) Abs for 4h or 8h. Equal amounts of RNA were assayed for gene expression using Affymetrix mouse 430 2.0 arrays.

2015-08-03 | E-GEOD-70393 | biostudies-arrayexpress

ZFP91 and IKZF1 Cooperatively Promote IMiD Resistance in T-Cell Lymphomas

Project description:The immunomodulatory (IMiD) agents, such as lenalidomide, are highly effective treatment for several B cell lymphomas but have poor efficacy in T cell lymphomas (TCLs). Here, we show that IKZF1 is a key drug target and vulnerability in lenalidomide sensitive TCL cells. However, TCLs are largely resistant and become less dependent on IKZF1. Instead, ZPF91 functions as a transcription factor (TF) and coregulates cell survival with IKZF1 in TCL cells that develop resistance to lenalidomide. Aberrant upregulation of CSNK2B, which leads to c-Jun inactivation, contributes to an enhanced TF activity of ZFP91 and suppresses immune activation triggered by lenalidomide. Although ZFP91 can be better targeted by pomalidomide compared to lenalidomide, an inefficient degradation of IKZF1 and ZFP91 widely exists among IMiD-resistance TCLs. A novel CELMoD agent CC-92480, with markedly increased potency and similar substrate selectivity, can overcome IMiD-resistance across multiple TCL subtypes by near complete degradation of IKZF1 and ZFP91.

2022-04-21 | GSE172505 | GEO

Expression data from cAMP-treated WT or IFN-gR1-deficient T cells

Project description:cAMP inhibits TCR signaling, T cell proliferation, cytokine production and T cell function. We used microarrays to detail the global programme of gene expression in TCR-activated WT or IFN-gR1-deficient CD4+ T cells by db-cAMP. CD4+ T cells were purified from spleens of WT or IFN-gR1-deficient mice by autoMACS, and activated with anti-CD3 plus anti-CD28 for 15 h. db-cAMP or vehicle control (med) was added into cultures for the last 3 h.

2012-07-23 | E-GEOD-39592 | biostudies-arrayexpress

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