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Unknown,Transcriptomics,Genomics,Proteomics

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Comparison of gene expression profiles of HIV-specific CD8 T cells from controllers and progressors and Jurkat cells with or without PD-1 ligation

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE24026: Comparison of gene expression profiles of Jurkat cells with or without PD-1 ligation GSE24081: Comparison of gene expression profiles of HIV-specific CD8 T cells from controllers and progressors Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: W. Haining

PROVIDER: E-GEOD-24082 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional analysis of HIV-specific CD8+ T cells shows that PD-1 inhibits T cell function by upregulating BATF.

Quigley Michael M Pereyra Florencia F Nilsson Björn B Porichis Filippos F Fonseca Catia C Eichbaum Quentin Q Julg Boris B Jesneck Jonathan L JL Brosnahan Kathleen K Imam Sabrina S Russell Kate K Toth Ildiko I Piechocka-Trocha Alicja A Dolfi Douglas D Angelosanto Jill J Crawford Alison A Shin Haina H Kwon Douglas S DS Zupkosky Jennifer J Francisco Loise L Freeman Gordon J GJ Wherry E John EJ Kaufmann Daniel E DE Walker Bruce D BD Ebert Benjamin B Haining W Nicholas WN

Nature medicine 20101003 10

CD8(+) T cells in chronic viral infections such as HIV develop functional defects including loss of interleukin-2 (IL-2) secretion and decreased proliferative potential that are collectively termed 'exhaustion'. Exhausted T cells express increased amounts of multiple inhibitory receptors, such as programmed death-1 (PD-1), that contribute to impaired virus-specific T cell function. Although reversing PD-1 inhibition is therefore an attractive therapeutic strategy, the cellular mechanisms by whic ...[more]

PMID: 20890291

Similar Datasets

Comparison of gene expression profiles of Jurkat cells with or without PD-1 ligation

Project description:CD8+ T cells in chronic viral infections like HIV develop functional defects such as loss of IL-2 secretion and decreased proliferative potential that are collectively termed exhaustion1. Exhausted T cells express increased levels of multiple inhibitory receptors, such as Programmed Death 1 (PD-1). PD-1 inhibition contributes to impaired virus-specific T cell function in chronic infection because antibody-mediated blockade of its ligand, Programmed Death Ligand 1 (PD-L1) is sufficient to improve T cell function and reduce viral replication in animal models. Reversing PD-1 inhibition is therefore an attractive therapeutic target, but the cellular mechanisms by which PD-1 ligation results in T cell inhibition are not fully understood. PD-1 is thought to limit T cell activation by attenuating T cell receptor (TCR) signaling. It is not known whether PD-1 ligation also acts by upregulating genes in exhausted T cells that impair their function. Here, we analyzed gene-expression profiles from HIV-specific CD8+ T cells in patients with HIV and show that PD-1 coordinately upregulates a program of genes in exhausted CD8+ T cells from humans and mice. This program includes upregulation of basic leucine transcription factor, ATF-like (BATF), a transcription factor in the AP-1 family. Enforced expression of BATF was sufficient to impair T cell proliferation and cytokine secretion, while BATF knockdown reduced PD-1 inhibition. Silencing BATF in CD4+ and CD8+ T cells from chronic viremic patients rescued HIV-specific T cell function. Thus inhibitory receptors can cause T cell exhaustion by upregulating genes â such as BATF â that inhibit T cell function. PD-1 expressing Jurkat cells were cultured for 18 hours with beads coated with antibodies to CD3 and CD28, with our without an antibody to PD-1.

2010-10-03 | E-GEOD-24026 | biostudies-arrayexpress

Comparison of gene expression profiles of HIV-specific CD8 T cells from controllers and progressors

Project description:CD8+ T cells in chronic viral infections like HIV develop functional defects such as loss of IL-2 secretion and decreased proliferative potential that are collectively termed exhaustion1. Exhausted T cells express increased levels of multiple inhibitory receptors, such as Programmed Death 1 (PD-1). PD-1 inhibition contributes to impaired virus-specific T cell function in chronic infection because antibody-mediated blockade of its ligand, Programmed Death Ligand 1 (PD-L1) is sufficient to improve T cell function and reduce viral replication in animal models. Reversing PD-1 inhibition is therefore an attractive therapeutic target, but the cellular mechanisms by which PD-1 ligation results in T cell inhibition are not fully understood. PD-1 is thought to limit T cell activation by attenuating T cell receptor (TCR) signaling. It is not known whether PD-1 ligation also acts by upregulating genes in exhausted T cells that impair their function. Here, we analyzed gene-expression profiles from HIV-specific CD8+ T cells in patients with HIV and show that PD-1 coordinately upregulates a program of genes in exhausted CD8+ T cells from humans and mice. This program includes upregulation of basic leucine transcription factor, ATF-like (BATF), a transcription factor in the AP-1 family. Enforced expression of BATF was sufficient to impair T cell proliferation and cytokine secretion, while BATF knockdown reduced PD-1 inhibition. Silencing BATF in CD4+ and CD8+ T cells from chronic viremic patients rescued HIV-specific T cell function. Thus inhibitory receptors can cause T cell exhaustion by upregulating genes â such as BATF â that inhibit T cell function. We sorted HIV-specific CD8+ T cells from 18 progressors and 24 controllers, cohorts with a two-log difference in mean viral load

2010-10-03 | E-GEOD-24081 | biostudies-arrayexpress

CD39 expression identifies terminally exhausted CD8+ T cells

Project description:Exhausted T cells express multiple co-inhibitory molecules that impair their function and limit immunity to chronic viral infection. Defining novel markers of exhaustion is important both for identifying and potentially reversing T cell exhaustion. Herein, we show that the ectonucleotidse CD39 is a marker of exhausted CD8+ T cells. CD8+ T cells specific for HCV or HIV express high levels of CD39, but those specific for EBV and CMV do not. CD39 expressed by CD8+ T cells in chronic infection is enzymatically active, co-expressed with PD-1, marks cells with a transcriptional signature of T cell exhaustion and correlates with viral load in HIV and HCV. In the mouse model of chronic Lymphocytic Choriomeningitis Virus infection, virus-specific CD8+ T cells contain a population of CD39high CD8+ T cells that is absent in functional memory cells elicited by acute infection. This CD39high CD8+ T cell population is enriched for cells with the phenotypic and functional profile of terminal exhaustion. These findings provide a new marker of T cell exhaustion, and implicate the purinergic pathway in the regulation of T cell exhaustion. CD8+ T cells from subjects with HCV infection were sorted and pelleted and re-suspended in TRIzol (Invitrogen). RNA extraction was performed using the RNAdvance Tissue Isolation kit (Agencourt). Concentrations of total RNA were determined with a Nanodrop spectrophotometer or Ribogreen RNA quantification kits (Molecular Probes/Invitrogen). RNA purity was determined by Bioanalyzer 2100 traces (Agilent Technologies). Total RNA was amplified with the WT-Ovation Pico RNA Amplification system (NuGEN) according to the manufacturer's instructions. After fragmentation and biotinylation, cDNA was hybridized to HG-U133A 2.0 microarrays (Affymetrix).

2015-09-08 | E-GEOD-72752 | biostudies-arrayexpress

FACS-sorted cells from Young Adults Vaccinated with Influenza TIV or LAIV Vaccines during 2008/09 Flu Season

Project description:Systems vaccinology has emerged as an interdisciplinary field that combines systems wide measurements and network and predictive modeling applied to vaccinology. Here we used the systems vaccinology approach to study the molecular mechanisms underlying the innate responses to the trivalent inactivated influenza (TIV) and live attenuated influenza (LAIV) vaccination in humans, and to identify early gene signatures that predict the magnitude of the antibody responses to influenza vaccination. During the 2008 influenza season, healthy adults were vaccinated with TIV (6 vaccinees) or LAIV (6 vaccinees), and blood samples isolated at day 0 and at day 7 post-vaccination. Cell subsets (B cells, Monocytes, mDCs and pDCs) were FACS-sorted from frozen PBMCs. Microarrays were performed using amplified total RNA.

2011-07-10 | E-GEOD-29618 | biostudies-arrayexpress

Systems biology of vaccination for seasonal influenza in humans

Project description:This SuperSeries is composed of the following subset Series: GSE29614: Time Course of Young Adults Vaccinated with Influenza TIV Vaccine during 2007/08 Flu Season GSE29615: Time Course of Young Adults Vaccinated with Influenza LAIV Vaccine during 2008/09 Flu Season GSE29617: Time Course of Young Adults Vaccinated with Influenza TIV Vaccine during 2008/09 Flu Season GSE29618: FACS-sorted cells from Young Adults Vaccinated with Influenza TIV or LAIV Vaccines during 2008/09 Flu Season Refer to individual Series

2011-07-10 | E-GEOD-29619 | biostudies-arrayexpress

PD-1 interacting proteins in Jurkat cells stimulated with Raji cells and SEE - Part3

Project description:Identifying PD-1 interacting proteins in Jurkat cells expressing PD-1 after stimulation with Raji cells and the superantigen SEE.

2019-05-06 | PXD010864 | Pride

PD-1 interacting proteins in SILAC labelled Jurkat cells stimulated with Raji cells - Part4

Project description:Identifying PD-1 interacting proteins in Jurkat cells expressing PD-1 after stimulation with Raji cells and the superantigen SEE.

2019-05-06 | PXD013531 | Pride

Profiling of naÃ¯ve and memory Tregs

Project description:Changes in Treg function are difficult to quantify due to the lack of Treg-exclusive markers in humans and the complexity of functional experiments. We sorted naive and memory human Tregs and conventional T cells, and identified genes that identify human Tregs regardless of their state of activation. We developed this Treg signature using Affymetrix human genome U133A 2.0 microarrays. To generate Tregs and Tconvs in multiple states of activation, naÃ¯ve (CD4+CD25hiCD45RA+) and memory (CD4+CD25hiCD45RA-) Tregs, and naÃ¯ve (CD4+CD25-CD45RA+) and memory (CD4+CD25-CD45RA-) Tconvs were sorted from blood of 7 healthy adults and RNA was isolated ex vivo or after stimulation for 40h, promoting activation-induced FOXP3 in Tconvs. The gene-expression profile of the eight cell subsets was analyzed. 7 adult healthy control samples were sorted into 4 subsets: naÃ¯ve (CD4+CD25hiCD45RA+) and memory (CD4+CD25hiCD45RA-) Tregs, and naÃ¯ve (CD4+CD25-CD45RA+) and memory (CD4+CD25-CD45RA-) Tconvs. These were used for RNA ex vivo and after 40h stimulation with anti-CD3/CD28 beads to induce an activation phenotype.

2016-01-19 | E-GEOD-76598 | biostudies-arrayexpress

Total and cholera toxin B-tetramer specific T cells from Peyer's patches and mesenteric lymph nodes

Project description:T cells were separately isolated from MLN and PP from two naive mice, and T cells binding to a cholera toxin B subunit specific MHC II tetramer from mice orally immunized with cholera toxin 7 days or boosted 5 days with a second dose of cholera toxin. Cells were purified using flow cytometric cell sorting and 3´ (n=5) or 5´ (n=5) libraries were constructed using the 10X workflow. From 5´libraries TCR libraries were also constructed and sequenced.

2022-06-22 | E-MTAB-11805 | biostudies-arrayexpress

RNA-seq data of lung resident T-cells from mice following house dust mite (HDM) sensitisation and subsequent influenza virus challenge

Project description:This data is from a murine model established to study the lasting impact of allergic airway sensitization on subsequent anti-viral memory T cell responses and the ability to develop protective immunity to reinfection. Animals were either sensitised by exposure to HDM or PBS and then subsequently exposed to influenza virus. Samples were collected at various time points for analysis of both CD8 and C4 positive tissue resident memory T cells.

2023-01-30 | E-MTAB-11116 | biostudies-arrayexpress

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