Defining the molecular mechanisms underlying immunological memory in T cells
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ABSTRACT:
PROVIDER: PRJNA279993 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1947710.fastq.gz | Fastqsanger.gz | |||
| SRR1947870.fastq.gz | Fastqsanger.gz | |||
| SRR1947711.fastq.gz | Fastqsanger.gz | |||
| SRR1947871.fastq.gz | Fastqsanger.gz | |||
| SRR1947712.fastq.gz | Fastqsanger.gz |
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Project description:Immunological memory is a defining feature of animal development, allowing rapid responses to repeat infections, yet the very basis of T cell-dependent memory remains poorly understood. Here we demonstrate that the critical steps in the acquisition of T cell memory occur not after completion of T cell differentiation but during the initial activation phase of naïve T cells, when extensive chromatin remodelling reprograms immune response genes towards a stably maintained primed state. During this process, inducible factors including AP-1 create hundreds of DNase I hypersensitive sites (DHSs), allowing the recruitment of ETS1 and RUNX1 to sites that were previously inaccessible. Significantly, these DHSs remain temporally and mitotically stable long after cessation of AP-1 activation, and function to maintain regions of active chromatin in the vicinity of genes that regulate immune responses. This priming enables increased accessibility and the accelerated induction of other inducible regulatory elements in previously activated T cells.
2016-02-02 | GSE67464 | GEO
Project description:Immunological memory is a defining feature of animal development, allowing rapid responses to repeat infections, yet the very basis of T cell-dependent memory remains poorly understood. Here we demonstrate that the critical steps in the acquisition of T cell memory occur not after completion of T cell differentiation but during the initial activation phase of naïve T cells, when extensive chromatin remodelling reprograms immune response genes towards a stably maintained primed state. During this process, inducible factors including AP-1 create hundreds of DNase I hypersensitive sites (DHSs), allowing the recruitment of ETS1 and RUNX1 to sites that were previously inaccessible. Significantly, these DHSs remain temporally and mitotically stable long after cessation of AP-1 activation, and function to maintain regions of active chromatin in the vicinity of genes that regulate immune responses. This priming enables increased accessibility and the accelerated induction of other inducible regulatory elements in previously activated T cells.
2016-02-02 | GSE67451 | GEO
Project description:Immunological memory is a defining feature of animal development, allowing rapid responses to repeat infections, yet the very basis of T cell-dependent memory remains poorly understood. Here we demonstrate that the critical steps in the acquisition of T cell memory occur not after completion of T cell differentiation but during the initial activation phase of naïve T cells, when extensive chromatin remodelling reprograms immune response genes towards a stably maintained primed state. During this process, inducible factors including AP-1 create hundreds of DNase I hypersensitive sites (DHSs), allowing the recruitment of ETS1 and RUNX1 to sites that were previously inaccessible. Significantly, these DHSs remain temporally and mitotically stable long after cessation of AP-1 activation, and function to maintain regions of active chromatin in the vicinity of genes that regulate immune responses. This priming enables increased accessibility and the accelerated induction of other inducible regulatory elements in previously activated T cells.
2016-02-02 | GSE67443 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2016-02-02 | GSE67465 | GEO
Project description:This a model from the article:
Evolution of immunological memory and the regulation of competition between
pathogens.
Wodarz D. Curr Biol
2003 Sep 16;13(18):1648-52 13678598
,
Abstract:
Memory is a central characteristic of immune responses. It is defined as an
elevated number of specific immune cells that remain after resolution of
infection and can protect the host against reinfection. The evolution of
immunological memory is subject to debate. The advantages of memory discussed so
far include protection from reinfection, control of chronic infection, and the
transfer of immune function to the next generation. Mathematical models are used
to identify a new force that can drive the evolution of immunological memory:
the duration of memory can regulate the degree of competition between different
pathogens. While a long duration of memory provides lasting protection against
reinfection, it may also allow an inferior pathogen species to persist. This can
be detrimental for the host if the inferior pathogen is more virulent. On the
other hand, a shorter duration of memory ensures that an inferior pathogen
species is excluded. This can be beneficial for the host if the inferior
pathogen is more virulent. Thus, while in the absence of pathogen diversity
memory is always expected to evolve to a long duration, under specific
circumstances, memory can evolve toward shorter durations in the presence of
pathogen diversity.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Wodarz D. (2003) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.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.
2024-09-02 | BIOMD0000000684 | BioModels
Project description:Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe expression profile of peritoneal macrophages from wild-type mice pre-administrated with TLR ligands or from ATF7 knockout mice. ATF7 suppresses a group of innate-immunity genes in macrophage by recruiting H3K9 dimethyltransferase G9a. TLR ligands induce ATF7 phosphorylation, leading to release of ATF7 from chromatin and reduction in H3K9me2 level. Partially disrupted chromatin structure and increased basal expression on target genes are maintained for a long period, increasing resistance pathogens. Therefore we speculate ATF7 is important factor in controlling innate immunological memory. This series contains seven sets of exression array data. For all sample, we use four CEL files generated by four biological-independent experiments.
2015-08-31 | E-GEOD-71111 | biostudies-arrayexpress
Project description:Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe 3,811 ATF7 binding sites in mouse peritoneal macrophages, and 95% of the ATF7 signals in wild-type macrophages are lost in ATF7 knockout macrophages. ATF7 suppresses a group of innate-immunity genes in macrophage by recruiting H3K9 dimethyltransferase G9a. TLR ligands induce ATF7 phosphorylation, leading to release of ATF7 from chromatin and reduction in H3K9me2 level. Partially disrupted chromatin structure and increased basal expression on target genes are maintained for a long period, increasing resistance pathogens. Therefore we speculate ATF7 is important factor in controlling innate immunological memory. This series contains one set of whole genome ChIP-chip data and 2 sets of promoter array ChIP-chip data. For all sample, we use three IP .CEL files and three WCE .CEL files (they are triplicated experiments) to make one profile.
2015-08-31 | E-GEOD-71112 | biostudies-arrayexpress
Project description:Human CD127 negative ILC2s show immunological memory.
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Project description:Immunological memory diversity in the human upper airway
| PRJNA1127438 | ENA
Project description:Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe expression profile of peritoneal macrophages from wild-type mice pre-administrated with TLR ligands or from ATF7 knockout mice. ATF7 suppresses a group of innate-immunity genes in macrophage by recruiting H3K9 dimethyltransferase G9a. TLR ligands induce ATF7 phosphorylation, leading to release of ATF7 from chromatin and reduction in H3K9me2 level. Partially disrupted chromatin structure and increased basal expression on target genes are maintained for a long period, increasing resistance pathogens. Therefore we speculate ATF7 is important factor in controlling innate immunological memory.
2015-08-31 | GSE71111 | GEO