Gene expression profile of TCR Vdelta1 positive gammadelta T cells expressed CD161
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Seiji Segawa
PROVIDER: E-GEOD-43402 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:To elucidate the difference between CD161-negative TCR Vdelta1 and CD161-positive TCR Vdelta1 cells, we performed GeneChip analysis of these two types of cells in peripheral blood mononuclear cells from healthy donors. Such analysis identified 192 genes that were expressed at two-fold or higher levels on CD161-positive TCR Vdelta1 cells than on CD161-negative TCR Vdelta1 cells. Expression of three genes (CCL3, CCL4 and CD161) from this signature was quantified in the same RNA samples by real-time PCR.
2014-01-09 | GSE43402 | GEO
Project description:Gene expression profiling of human CD8+ CD161hi and CD161lo central and effector memory and naïve T cell subsets. The mechanisms by which IL-17 secreting cells are regulated have not been completely elucidated. We previously identified a population of rhodamine-effluxing memory CD8+ T cells with high expression of CD161 that contributes to immune reconstitution after lymphopenia-inducing chemotherapy. Here we find that CD161hi CD8+ T cells share transcriptional programming with Th17 cells, but most do not secrete IL-17 or proliferate to stimulation through the T cell receptor (TCR). Transcriptional analysis of subsets identified by expression of CD161 and CD62L revealed a novel mechanism of TCR signaling pathway regulation in CD161hi CD8+ T cells that is distinct from that described in anergic or tolerant cells and renders them functionally dependent on costimulation through innate cytokine receptors or CD28. CD161hi CD8+ T cells, induced to proliferate by a TCR signal delivered with costimulation, demonstrated plasticity that was dependent on the nature of costimulation and resulted in expansion of IL-17 secreting cells that could not proliferate to a TCR signal alone or differentiation to Tc1-like cells that proliferated to TCR stimulation in the absence of costimulation. The data show an association between TCR signaling pathway downregulation and type 17 programming in CD161hi CD8+ T cells, whose dysregulation could mediate IL-17 dependent inflammatory diseases. T cell subsets were sort-purified from healthy adults and analyzed by gene expression profiling. Isolation: Effluxing CD161hi and non-effluxing CD161lo CD8+ TCM and TEM subsets were purified using magnetic bead separation and cell sorting to achieve >98% purity, as previously described (35). CD8+ T cells were positively selected using CD8 Microbeads (Miltenyi Biotec, Germany), loaded with Rh123 (Sigma, St. Louis, MO) and cultured for 30 min to allow Rh123 efflux, then labeled with fluorochrome-conjugated antibodies to CD4, CD16, TCRγδ, Vα24, CD8, CD95, CD62L and CD161. CD161hi and CD161lo TCM and TEM subsets were sort-purified on a FACS ARIA equipped with 405 nm, 488 nm and 633 nm lasers (BD Biosciences). CD161hi TCM and TEM subsets were identified as CD62L+/Rh123lo/CD161hi and CD62L-/Rh123lo/CD161hi events, respectively, in the CD4-/CD16-/TcRγδ-/Vα24-/CD8+/CD95+ population. CD161lo TCM and TEM subsets were identified as CD62L+/Rh123hi/CD161int/neg and CD62L-/Rh123hi/CD161int/neg events, respectively, in the CD4-/CD16-/TcRγδ-/Vα24-/CD8+/CD95+ population. Gene expression profiling: RNA was extracted from sort-purified subsets from 6 healthy individuals using the RNeasy Plus Minikit (Qiagen, Valencia, CA) and biotinylated, followed by generation of amplified cRNA for array hybridization using the Illumina TotalPrep RNA Amplification Kit (Applied Biosystems, Foster City, CA). Amplified biotinylated cRNA was then purified before quality control to ensure high quality cRNA was available for hybridization. Labeled cRNA was hybridized to Illumina WG-6 Expression BeadChips v3.0 (Illumina, San Diego, CA), which quantitate expression of 48,802 transcripts derived from the NCBI RefSeq (Build 36.2, Release 22) and UniGene databases (Build 199). BeadChips were washed before reading and image extraction, and then scanned on an Illumina BeadArray Reader. The resulting TIFF images were processed using GenomeStudio Gene Expression Module (GEM) software. Data quality was assessed using the Control Summary feature in GenomeStudio GEM. For a given analysis set, a GenomeStudio Probe-level Final Report was generated by combining the Sample Probe Profile and Control Probe Profile tables. The Final Report comprising the full dataset was initially processed using the Bioconductor package lumi by employing a background correction estimate and quantile normalization. A small adjustment (i.e. 20 counts) was made to the entire dataset to make all intensity signals non-negative and these values were log2-transformed. The dataset was initially filtered using the ‘shorth’ function of the Bioconductor package genefilter, resulting in retention of 31,084 of 48,802 original probes. Each pairwise comparison was further filtered by discarding probes whose signal intensity was less than a defined signal “noise floor” across all arrays in the data subset. This was achieved by calculating the median of the ‘negative control’ probe signals for each array, averaging these values, and setting the noise floor as 3 times this average. Differential gene expression was then determined using the Bioconductor package limma, and a false discovery rate (FDR) method applied to correct for multiple testing. Significant differential gene expression was defined by a log2 ratio > 0.585 (± 1.5-fold) and FDR (adjusted p value) < 0.05.
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Project description:Gene expression profile of TCR Vdelta1 positive gammadelta T cells expressed CD161
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Project description:In this study, we examined differential gene expression in naïve human CD4+ T cells, as well as in effector Th1, Th17-negative and Th17-enriched CD4- T cell subsets. We observed a marked enrichment for increased gene expression in effector CD4+ T cells compared to naive CD4+ among immune-mediated disease oci genes. Within effector T cells, expression of disease-associated genes was increased in Th17-enriched compared to Th17-negative cells. We used microarray to examine the gene expresssion profile and level of human naïve, Th1 and effector T cell subsets. Human PBMCs were isolated and sorted to naïve, CD161-CCR6- and CD161+CCR6+ memory T cells. Naïve T cells were differentiatied to Th1 cells, and CD161-CCR6- and CD161+CCR6+ memory T cells were in vitro expanded for Th17-negative and Th17-enriched effector T cells. The gene profile was compared among naive, Th1, Th17-negative, and Th17-enriched cell subsets.
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Project description:We have employed whole microRNA microarray with the potential to distinguish H.pylori infection.Among the 470 human miRNAs represented on the array chip, 228 were undetectable or expressed below the background and so were eliminated, leaving 242 miRNAs for the supervised analysis. When comparing 10 H. pylori-negative and nine H. pylori-positive subjects, 55 miRNAs were deemed significantly different on the basis of microRNA arrays. During endoscopy, a biopsy specimen was obtained from the gastric antrum along the lesser curvature. Biopsies of 10 H. pylori-negative and nine H. pylori-positive patients' subjects were performed.Exclusion criteria were: age <18 or >80 y, pregnancy, body mass index (BMI) >30 kg/m2, diabetes mellitus, cachectic state (including cancer), systemic infection, liver disease, renal impairment, use of medications effective against H. pylori during the preceding 3 months, alcohol abuse, drug addiction, and chronic corticosteroid or nonsteroidal anti-inflammatory drug use. None of the subjects had undergone gastrointestinal surgery.
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Project description:The aim of the dataset was to study on a genome-wide level the impact of Lat deficiency on gene expression in resting and activated CD4+ T cells Lat+ and Lat? CD4+ T cells were isolated from lymph nodes and spleen of Latfl-dtr Tmat-Cre mice using a Dynabeads untouched mouse CD4 cells kit (Life Technology) and further purified by cell sorting. Lat+ CD4+ T cells were defined as: CD5+, hDTR+, CD8?, TCR???, CD25?, CD69?, CD62L+, lineage (CD11c, CD11b, CD19, CD45R, CD161)? and Lat? CD4+ Tcells were defined as: CD5+, hDTR?, CD8?, TCR???, CD25?, CD69?, CD62L+, lineage (CD11c, CD11b, CD19, CD45R, CD161)?. Sorted Lat+ or Lat? CD4+ T cells were then kept in vitro for 4 hours without stimulation or activated for 4 hours using anti-CD3 antibody and anti-CD28 antibody. Cell samples corresponding to three biological replicates were analyzed and gene expression profiles were obtained from total RNA.
2014-03-02 | E-GEOD-49507 | biostudies-arrayexpress
Project description:We used microarray to compare gene expression between CD161++/CD161+/CD161-CD8+ T cells from human cord blood. Lymphocytes from freshly obtained human cord blood samples were isolated by Ficoll density centrifugation. CD8+ T cells were purified by negative selection using magnetic beads and subsequently labelled with fluorescent antibodies prior to sorting using MoFlo MLS cell sorter (Dako).
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Project description:Type I interferons (IFNs) play a key role in linking the innate and adaptive immune responses. IFNs can have both positive and negative effects on the development of memory CD8+ T cells, but their contribution to the priming of naïve T cells is unclear. Using OT-I TCR transgenic T cells, we show strong effects on TCR-induced functional response when sensitized by IFN-β prior to their stimulation with cognate antigen. These effects are only seen in the absence of co-stimulation and at suboptimal TCR stimulation conditions. Pre-stimulation of naïve T cells inhibits certain TCR-mediated functions like cell proliferation and the induction of genes such as IFN-γ and IL-2. However, type I IFN does not influence the induction of other TCR-induced functions like the expression of the T cell activation marker CD25 and a number of other genes. IFN-mediated impairment of proliferation is due to the lack of IL-2 induction since it can be compensated by exogenous IL-2. Further analysis reveals an IFN-mediated inhibition of Ca2+ flux and ERK phosphorylation. In vivo studies confirm that pre-stimulation with IFNs inhibits early T cell responses, whereas long-term responses are positively affected. Our results reveal that IFN exerts negative effects on naïve T cells in a timely defined range under sub-optimal TCR stimulation conditions. These results highlight the importance of timing of immune-regulatory events and reveal a novel role for type I IFNs by shaping the immune response, such that T cells are not able to react until optimal stimulation is provided. 8 Arrays, untreated cells as references, IFNb treatment and/or TCR stimulation at various lengths of time
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Project description:Background. T cells in the thymus undergo opposing positive and negative selection processes so that the only T cells entering circulation are those bearing a T cell receptor (TCR) with a low affinity for self. The mechanism differentiating negative from positive selection is poorly understood, despite the fact that inherited defects in negative selection underlie organ-specific autoimmune disease in AIRE-deficient people and the non obese diabetic (NOD) mouse strain. Results. Here we use homogeneous populations of T cells undergoing either positive or negative selection in vivo together with genome-wide transcription profiling on microarrays to identify the gene expression differences underlying negative selection to an Aire-dependent organ-specific antigen, including the upregulation of a genomic cluster in the cytogenetic band 2F. Analysis of defective negative selection in the autoimmune-prone NOD strain demonstrates a global impairment in the induction of the negative selection response gene set, but little difference in positive selection response genes. Combining expression differences with genetic linkage data we identify differentially expressed candidate genes including Bim, Bnip3, Smox, Pdrg1, Id1, Pdcd1, Ly6c, Pdia3, Trim30 and Trim12. Conclusions. The data provide a molecular map of the negative selection response in vivo, and by analysis of deviations from this pathway in the autoimmune susceptible NOD strain, suggest that susceptibility arises from small expression differences in genes acting at multiple points in the pathway between the TCR and cell death. Experiment Overall Design: Analysis of two thymic populations - early single positive thymocytes (CD4+CD8lowCD69+TCRhi) and early double positive thymocytes (CD4+CD8+CD69-TCRlow). Samples purified from the 3A9 TCR transgenic (TCR) to characterise positive selection and the 3A9 TCR x insHEL double transgenic (Dbl) to characterise negative selection towards an Aire-dependent organ-specific antigen. Both the non autoimmune C57BL10.H2k (B10) and autoimmune Non obese diabetic (NOD) strains were analysed in this method. Three biological replicates were used for each of these eight different groups.
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