TCR Repertoire of CD4+ T cells in Human Lymph Nodes
Ontology highlight
ABSTRACT:
REPOSITORIES: dbGaP
Similar Datasets
Project description:The High dimensional analyses of CD4+ T cells in human lymph nodes is a case-based analysis of the TCR repertoire, transcriptome, and epigenetic signatures of various CD4+ T cells in human lymph nodes. The study aims to determine clonal overlap between phenotypically distinct CD4+ T cells and the similarities between these populations on transcriptional and epigenetic levels. This study performs TCR repertoire sequencing using Molecular Identifier Clustering-based Immune Repertoire Sequencing (MIDCIRS). We found clonal overlap between a population of CXCR5- T cells and Tfh cells. We also show epigenetic and transcriptional similarities between CXCR5-PD-1+ T cells and Tfh cells.
| phs001849 | dbGaP
Project description:TCR Repertoire of CD4+ T cells in Human Lymph Nodes
| PRJNA434344 | ENA
Project description:TCR Repertoire of CD4+ T cells in Human Lymph Nodes
| PRJNA434343 | ENA
Project description:Cell activation is a vital step for T cell memory/effector differentiation as well as for productive HIV infection. To identify novel regulators of this process, we used next generation sequencing to profile changes in microRNA expression occurring in purified human naive CD4 T cells in response to TCR stimulation and HIV infection. HIV infection had no significant impact on global miR expression in quiescent nave CD4 T cells. We identified miR-34c-5p as a novel miR strongly induced by TCR stimulation of nave CD4 T cells, and found that it was consistently down-regulated in response to viral infection. Over-expression of miR-34c-5p had a positive effect on HIV-1 replication. Finally, we demonstrated that miR-34c-5p alters the expression of several genes involved in TCR signaling and cell activation, identifying it as a novel regulator of nave CD4 T cell activation potentially targeted by HIV infection.
2016-12-21 | E-MTAB-4214 | ArrayExpress
Project description:To investigate the influence of CNS3, a cis-regulatory element in the Foxp3 locus, on the selection of T cell antigen receptor (TCR) repertoire of regulator CD4+ T cells (Treg), we crossed Foxp3ΔCNS3-gfp or control Foxp3gfp mice to DO11.10 TCRβ transgene and Tcra-/+ background. We isolated Treg and conventional CD4+T cells from thymus, spleen and lymph nodes of Foxp3ΔCNS3-gfp DO11.10 TCRβ Tcra-/+ or Foxp3gfp DO11.10 TCRβ Tcra-/+ male littermates, and sequenced the TCRα chains. Analysis of the diversity of Complementary Determining Region 3 (CDR3) of TCRα showed a distinct clustering of CNS3-deficient Treg cells from the CNS3-sufficient ones. Overall design: DO11.10 TCRβ transgene inhibits the recombination of endogenous Tcrb loci thus restricting TCR repertoire to TCRα chains expressed by T cells. Further limitation of the TCR repertoire was achieved by the presence of one functional Tcra gene. With restricted TCR repertoire, mRNA of TCRα was extracted from Treg and conventional CD4+ T cells for library preparation and high throughput sequencing.
| GSE71162 | GEO
Project description:This study set out to examine CD4 T cell differentiation in a mouse model of diabetes based on transgenic expression of ovalbumin under the control of the rat insulin promoter and co-expression of the DO11.10 transgene (DO11 x rip-mOVA mice). The transcriptome of T cells isolated from the pancreatic lymph nodes (lymph nodes draining the site of self antigen expression) was compared with that of T cells isolated from inguinal lymph nodes (non-draining lymph nodes). T cells were sorted based on expression of CD4, DO11.10 TCR (KJ-126), CD25 and CD69. Primary cells from 6 week old DO11 x rip-mOVA mice were isolated ex-vivo from the pancreatic lymph nodes or inguinal lymph nodes. Cells were sorted by flow cytometry using antibodies to CD4, DO11.10 TCR (KJ-126+), CD25 and CD69. 3-6 replicates were collected per experimental group with each replicate deriving from 14 mice. RNA was isolated using the RNeasy micro kit (Qiagen).
2014-10-07 | E-GEOD-62104 | ArrayExpress
Project description:This a model from the article:
Modeling defective interfering virus therapy for AIDS: conditions for DIV
survival.
Nelson GW, Perelson AS. Math Biosci
1995 Feb;125(2):127-53 7881191
,
Abstract:
The administration of a genetically engineered defective interfering virus (DIV)
that interferes with HIV-1 replication has been proposed as a therapy for HIV-1
infection and AIDS. The proposed interfering virus, which is designed to
superinfect HIV-1 infected cells, carries ribozymes that cleave conserved
regions in HIV-1 RNA that code for the viral envelope protein. Thus DIV
infection of HIV-1 infected cells should reduce or eliminate viral production by
these cells. The success of this therapeutic strategy will depend both on the
intercellular interaction of DIV and HIV-1, and on the overall dynamics of virus
and T cells in the body. To study these dynamical issues, we have constructed a
mathematical model of the interaction of HIV-1, DIV, and CD4+ cells in vivo. The
results of both mathematical analysis and numerical simulation indicate that
survival of the engineered DIV purely on a peripheral blood HIV-1 infection is
unlikely. However, analytical results indicate that DIV might well survive on
HIV-1 infected CD4+ cells in lymphoid organs such as lymph nodes and spleen, or
on other HIV-1 infected cells in these organs.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Nelson GW, Perelson AS. (1995) - version=1.0
The original CellML model was created by:
Ethan Choi
mcho099@aucklanduni.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230081 | BioModels
Project description:This a model from the article:
Modeling defective interfering virus therapy for AIDS: conditions for DIV
survival.
Nelson GW, Perelson AS. Math Biosci
1995 Feb;125(2):127-53 7881191
,
Abstract:
The administration of a genetically engineered defective interfering virus (DIV)
that interferes with HIV-1 replication has been proposed as a therapy for HIV-1
infection and AIDS. The proposed interfering virus, which is designed to
superinfect HIV-1 infected cells, carries ribozymes that cleave conserved
regions in HIV-1 RNA that code for the viral envelope protein. Thus DIV
infection of HIV-1 infected cells should reduce or eliminate viral production by
these cells. The success of this therapeutic strategy will depend both on the
intercellular interaction of DIV and HIV-1, and on the overall dynamics of virus
and T cells in the body. To study these dynamical issues, we have constructed a
mathematical model of the interaction of HIV-1, DIV, and CD4+ cells in vivo. The
results of both mathematical analysis and numerical simulation indicate that
survival of the engineered DIV purely on a peripheral blood HIV-1 infection is
unlikely. However, analytical results indicate that DIV might well survive on
HIV-1 infected CD4+ cells in lymphoid organs such as lymph nodes and spleen, or
on other HIV-1 infected cells in these organs.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Nelson GW, Perelson AS. (1995) - version=1.0
The original CellML model was created by:
Ethan Choi
mcho099@aucklanduni.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230033 | BioModels
Project description:To activate primary T cells, lymph nodes were removed and disaggregated. Cells were cultured in RPMI 1640 containing L-glutamine, 10% FBS, 50 μM β-mercaptoethanol and penicillin/streptomycin. Cells were stimulated with 1 μg/ml of the CD3 monoclonal antibody (2C11) and 2 μg/ml anti-CD28 (37.51) in the presence of cytokines IL12 (10 ng/ml) and 20 ng/ml IL2 (20 ng/ml). Cells were stimulated for 24 hours. Live TCR activated CD4+ cells were sorted for CD4+ and CD45.1+ expression and DAP1 exclusion prior to collection for proteomics processing. Mice were “wild-type” (ie non-TCR transgenic) from OT-2 CD45.1 expressing C57bl6 background maintained in-house line.
2019-03-29 | PXD012052 | Pride
Project description:We were interested in investigating the heterogeneity of CD4+ Th2 cells during infection response. In order to do so we injected Nippostrongylus brasiliensis (Nb) in recipient mice as this is known to elicit a Type 2 response. Mice were subcutaneously injected with Nb larvae and single CD4+ cells were isolated from mediastinal lymph nodes, mesenteric lymph nodes, and lungs 5 days after infection.
2016-04-13 | E-MTAB-4619 | ArrayExpress