Ontology highlight
ABSTRACT:
PROVIDER: PRJNA633838 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11811762_1.fastq.gz | Fastqsanger.gz | |||
| SRR11811762_2.fastq.gz | Fastqsanger.gz | |||
| SRR11811763_1.fastq.gz | Fastqsanger.gz | |||
| SRR11811763_2.fastq.gz | Fastqsanger.gz | |||
| SRR11811764_1.fastq.gz | Fastqsanger.gz |
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Project description:CD4 T follicular helper (Tfh) cells provide the required signals to B cells for germinal center reactions that are necessary for longlived antibody responses. However, it remains unclear whether there are CD4+ memory T cells committed to the Tfh lineage after antigen clearance. Using adoptive transfer of antigen-specific memory CD4+ subpopulations (based on CXCR5 and Ly6c expression)in the LCMV infection model, we found that there are distinct memory CD4+ T cell populations with commitment to the Tfh and Th1 lineages. Our conclusions are based on gene expression profiles, epigenetic studies and phenotypic and functional analysis. The gene expression profiles of virus-specific CD4 T cell subets at effector and memory stages is presented here. The SMARTA TCR transgenic / adptive transfer system was used to identify and sort subsets of antigen-specific CD4 T cells (based on their expression of Ly6c and CXCR5) elicited after acute infection with LCMV (Arm).
2013-04-22 | E-GEOD-43863 | biostudies-arrayexpress
Project description:IL-2 inducible tyrosine kinase (Itk) is a Tec family non-receptor tyrosine kinase that is known to regulate T cell receptor signal strength (TcR) and T cell development and differentiation. TcR signal strength and antigen affinity are parameters known to regulate the development of CD8+ T cell memory. However, the intersection between TcR signal strength and antigen affinity on CD8+ memory T cell development remains unclear. Therefore, we compared the transcriptomes of WT and Itk-/- OT-1/Rag-/- CD8+ T cells at day 0 and day 7 following infection with Listeria monocytogenes expressing the SIINFEKL (N4) or SIITFEKL (T4) OVA peptide variant (different affinities for TcR) by RNA sequencing.
2020-09-30 | GSE137406 | GEO
Project description:Cognate antigen signals control CD8+ T cell priming, expansion size and effector versus memory cell fates, however, it is not clear whether they can also modulate the functional features of memory CD8+ T cells. We observed that OT-I cells that were primed with weak cognate antigen signals incorporate more cytokine signals, leading to a hypothesis that CD8+ T cells that receive weak TCR signals require cytokine signals to form functional memory. Using a previously described mouse model in which IL-2 signaling via its high affinity receptor CD25 is selectively impaired, the “Il2ramut/mut” mouse, we conducted a comparative analysis of gene expression and epigenetic landscape of Il2ramut/mut and WT OT-I memory cells that were primed with strong (Lm-Ova N4) versus weak (Lm-Ova T4). RNA seq data showed that both TCR and IL-2 priming signals have minimal effect on gene expression in resting memory CD8 T cells, but they significantly modify the epigenetic landscape of the memory CD8 T cells. These findings have important contributions to the current understanding of how priming signals program memory CD8 T cells in vivo.
2020-09-30 | GSE152392 | GEO
Project description:Much is known concerning the cellular and molecular basis for CD8+ T memory immune responses. Nevertheless, conditions that selectively support memory generation have remained elusive. Here we show that an immunization regimen that delivers TCR signals through a defined antigenic peptide, inflammatory signals through LPS, and growth and differentiation signals through the IL-2R initially favors antigen-specific CD8+ T cells to rapidly and substantially develop into tissue-residing T effector-memory cells by TCR transgenic OVA-specific OT-I CD8+ T cells. Amplified CD8+ T memory development depends upon a critical frequency of antigen-specific T cells and direct responsiveness to IL-2. A homologous prime-boost immunization protocol with transiently enhanced IL-2R signaling in normal mice led to persistent polyclonal antigen-specific CD8+ T cells that supported protective immunity to Listeria monocytogenes. These results identify a general approach for amplified T memory development that may be useful to optimize vaccines aimed at generating robust cell-mediated immunity. Gene expression analysis was performed for OT-I T cells on day 3 and day 5 after activation with ovalbumin and LPS in vivo with and without treatment with IL-2 using an agonists IL-2/anti-IL-2 complexes (IL2/Jes-6.1) OT-I T cells were purified and adoptively transferred into congenic syngenic mice. 24 hours later mice were immunization with ovalbumin and LPS. 24 hr later some mice received agonist IL2/anti-IL2. 3 and 5 days after immunization, the activated OT-I T cells were purifed by FACS and total RNA was isolated for genome wide expression analysis using Affymetrix Mouse Gene ST1.0 arrays
2012-10-03 | E-GEOD-39110 | biostudies-arrayexpress
Project description:Immune memory cells are poised to rapidly expand and elaborate effector functions upon reinfection. However, despite heightened readiness to respond, memory cells exist in a functionally quiescent state. The paradigm is that memory cells remain inactive due to lack of TCR stimuli. Here we report a unique role of Tregs in orchestrating memory quiescence by inhibiting effector and proliferation programs through CTLA-4. Loss of Tregs resulted in activation of genome-wide transcriptional programs characteristic of potent effectors, and both developing and established memory quickly reverted to a terminally differentiated (KLRG-1hi/IL-7R±lo/GzmBhi) phenotype, with compromised metabolic fitness, longevity, polyfunctionality and protective efficacy. CTLA-4, an inhibitory receptor overexpressed on Tregs, functionally replaced Tregs in trans to rescue Treg-less memory defects and restore homeostasis of secondary mediators as well. These studies present CD28-CTLA-4-CD80/CD86 axis as a novel target to potentially accelerate vaccine-induced immunity and improve T-cell memory quality in current cancer immunotherapies proposing transient Treg-depletion. We used microarray analysis to detail the global programming of gene expression in LCMV GP33-specific CD8 T cells differentiated in the presence or absence of regulatory T cells Differentiation of memory CD8 T cells entails a progressive transition of highly activated effector program to a quiescent memory program. A key question in the field is to understand the factors that aid in the differentiation of memory cells from effector cells. It is a generally accepted paradigm that effector cells transition to a memory state by default after antigen clearance, since TCR stimuli is the key driver of effector programs in CD8 T cells. We hypothesized that the effector to memory transition of CD8 T cells involves active immunological brakes through regulatory T cells (Tregs) that allow the highly activated effector cells to convert into quiescent memory cells. To address this hypothesis, we used FoxP3-DTR mice to deplete Tregs during the window following antigen clearance, during which the effector CD8 T cells convert to long-lived memory cells. To get a deeper understanding of the global transcriptome of CD8 T cells as they transition from an effector to a memory state, we isolated and arrayed the antigen-specific CD8 T cells at day 16 post-infection that have experienced the transitional environment with and without the presence of Tregs.
2015-06-16 | E-GEOD-67593 | biostudies-arrayexpress
Project description:Signaling through the T cell antigen receptor is essential for the formation of regulatory T (Treg) cells in the thymus and for their involvement in antigen-directed suppression of immune responses. Using a conditional null allele of the gene encoding p56Lck we show here that T cell antigen receptor (TCR) signaling is also essential for sustaining the phenotype and homeostasis of Treg cells. Inactivation of p56Lck in Treg cells resulted in large-scale changes in their gene expression profile, blocked their capacity to suppress responses, inhibited their proliferation, and caused them to redistribute in the body. The results make clear multiple aspects of the Treg cell phenotype that are dependent on a sustained capacity to respond through their TCRs. Keywords: Genetic deficiency of p56lck Two-condition experiment: wild-type memory or regulatory T cells versus lck-deficient memory or regulatory T cells.
2010-05-22 | E-GEOD-13645 | biostudies-arrayexpress
Project description:This lab investigates how protein-carbohydrate interactions affect cell fate in the immune system. The specific focus is on the mechanism of galectin-1 mediated death of T lymphocytes, and the role of galectin-1 in immune development, lymphocyte homeostasis, response to pathogens, autoimmunity and tumor cell evasion of the immune response. T cell memory, the ability of T cells to respond to recall antigens rapidly and effectively, is a critical component of the adaptive immune response and the essential target of vaccine development. After naive T cells are exposed to a new antigen (or pathogen), expansion of antigen-specific T cells creates an effector population; the majority of effector T cells die once the antigen or pathogen is cleared. A small subset of T cells remains after antigen is cleared, the memory T cells. These memory cells can respond more rapidly than naive cells to recall antigen, and are also capable of homeostatic self-renewal. During the development of T cell memory, there are dramatic changes in gene transcription, protein expression and post-translational modification of proteins, compared to naive and effector T cells. Our labs have described some of these changes at the phenotypic level, and have found important distinctions in the glycotypes of naive, effector and memory T cells. However, there has not been a systematic examination of differential glycosyltransferase expression among these T cell populations. Gene expression during the development of T-cell memory: After naive T cells are exposed to a new antigen (or pathogen), expansion of antigen-specific T cells creates an effector T cell population, the majority of which dies once antigen is cleared. A small subset, the memory T cells, remains after antigen is cleared. Using the LCMV system in P14 TCR transgenic mice specific for the DbGP33-41 epitope of LCMV, RNA (triplicate samples) was isolated from FACS-sorted virus-specific CD8+ T-cell populations during a time course following viral infection. The time points are day 0, day 8 (the peak of T-cell expansion following viral infection), day 15 (during the contraction or apoptotic phase), day 22 (during the transitional phase), and day 40 or later (the stable memory phase). The RNA samples were analyzed by Glyco-gene Chip analysis.
2011-01-07 | E-GEOD-26479 | biostudies-arrayexpress
Project description:We designed a lineage tracing method to label a wave of T cells produced in the thymus of young. TCR repertoire analysis revealed that the lineage-tracked CD4 memory-like T cells and T regulatory cells exhibited age-dependent enrichment of shared clonotypes, indicating that antigen matched T regulatory cells are involved in maintaining the tolerant status of long-lived T cell clones. Furthermore, these shared clonotypes were found across different mice maintained in the same housing condition mice. Examination of antigen-specificity of aging-tracking T-cell subtype.
2016-07-21 | E-GEOD-84438 | biostudies-arrayexpress
Project description:<p>Diversity and size of the antigen-specific T cell receptor (TCR) repertoire are two critical determinants for successful control of chronic infection. Varicella zoster virus (VZV) that establishes latency during childhood is able to escape control mechanisms, in particular with increasing age. We examined the TCR diversity of VZV-specific CD4 T cells in individuals older than 50 years by studying three identical twin pairs and three unrelated individuals before and after vaccination with live attenuated VZV. While all individuals had a small number of dominant T cell clones, the breadth of the VZV-specific repertoire differed markedly among different individuals. A genetic influence was seen for the sharing of individual TCR sequences from antigen-specific cells, but not for repertoire richness or the selection of clonal dominance. VZV vaccination favored the expansion of infrequent VZV-specific TCRs including those from naïve T cells while leaving dominant T cell clones mostly unaffected.</p>
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Project description:It is unclear to what extent T helper cells with a different phenotype (chemokine receptor and cytokine production profile) are generated in response to pathogen challenge or vaccination, and whether such heterogeneity can arise among the progeny of a single precursor. We combined cellular methods to isolate antigen specific T cells from different T helper memory subsets of human donors, and next generation sequencing of their TCR. This approach revealed a high level of heterogeneity in the phenotype of human T cells responding to different pathogens/vaccines also at a clonal level, as we could characterize cells bearing an identical T cell receptor with divergent effector properties. NGS-based analysis of T cell receptor repertoire of T helper memory cells identical gross specificity (i.e. responding to a given pathogen or vaccine antigen) belonging to different heper subsets (Th1, Th2, Th17)
2015-01-13 | E-GEOD-64852 | biostudies-arrayexpress