Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ScRNA-seq of mouse Plasmodium-specific TCR-transgenic CD4+ T cells prior to and after re-infection.

ABSTRACT: Naturally-acquired immunity to blood-stage malaria is associated with several effector CD4 + T subsets including germinal centre (GC) Tfh, Th1 and Tr1 cells. Children in malaria-endemic regions can experience repeated Plasmodium infections over short periods of time; yet the effect of reinfection on multiple co-existing effector and memory subsets remains unclear. Here, we tracked antigen-experienced TCR-transgenic CD4+ T cells during Plasmodium re-infection in mice using scRNA-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE233703 | GEO | 2024/05/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

scRNA-seq + TCR-seq of mouse polyclonal CD4+ T cells prior to and after re-infection.

Project description:Naturally-acquired immunity to blood-stage malaria is associated with several effector CD4 + T subsets including germinal centre (GC) Tfh, Th1 and Tr1 cells. Children in malaria-endemic regions can experience repeated Plasmodium infections over short periods of time; yet the effect of reinfection on multiple co-existing effector and memory subsets remains unclear. Here, we tracked antigen-experienced polyclonal CD4+ T cells during Plasmodium re-infection in mice using scRNA-seq/TCR-seq.

2024-05-02 | GSE233713 | GEO

Spatial transcriptomics of mouse spleens during malaria convalescence.

2024-05-02 | GSE234253 | GEO

Profiling the human immune response to Plasmodium falciparum during the first three infections of life

Project description:Controlled human malaria infection is a powerful experimental medicine tool to understand the human immune response to a first ever malaria infection. Here we have taken this approach a step further and conducted the first human malaria reinfection trial in the modern era. Volunteers were challenged up to three times with Plasmodium falciparum in 4- to 8-month intervals. Remarkably, parasite densities and the dynamics of blood-stage infection were not altered over the course of three homologous infections. Using whole blood RNA-sequencing we tracked the host immune response through time and found that the emergency myeloid response, which triggers systemic inflammation and the global recruitment of T cells into lymphoid tissues, is not altered by repeated infection. Six days after parasite clearance, when the innate response subsides, T cells return to the circulation and reflect the outcome of critical cell-cell interactions within the inflamed spleen. By transcriptionally profiling flow sorted CD4+ T cell subsets after their release from the tissue we could show that TH1 polarised effector response in naïve hosts is tolerised upon re-challenge to avoid collateral tissue damage. Instead, a subset of specialised cytokine-producing CD4+ T cells are activated to promote essential protective immune functions. Together these data indicate that innate and adaptive immune responses can be uncoupled in malaria and illustrate that human hosts prioritises damage limitation (tolerance) over parasite clearance (resistance) to quickly acquire clinical immunity.

2021-05-25 | GSE172481 | GEO

scRNA-seq mouse splenocytes prior to and during blood-stage malaria infection.

Project description:Blood-stage malaria infection induces differentiation of several effector CD4 + T subsets including Tfh and Th1 cells. The cues and microarchitectural niches required in secondary lymphoid organs for their formation were previously uncharacterised. Here we used scRNA-seq to profile splenocyte transcriptomes at steady state or upon malaria infection as a reference dataset for deconvolution of spatial transcriptomic data.

2024-07-08 | GSE244804 | GEO

Transcriptional profiling of CD4+ T cells activated in murine malaria.

Project description:CD4+ T cells are critical for defense against the Plasmodium parasites that cause malaria. To better understand CD4+ T cell effector mechanisms during malaria, we performed microarray analysis of CD4+ T cells from naïve and infected mice. Comparison of activated (CD44 hi CD62L lo) CD4+ T cells from infected mice to bulk CD4+ T cells from naïve mice revealed a subset of genes that were upregulated by infection with Plasmodium chabaudi. These results help generate a more complete picture of CD4+ T cell function in malaria.

2016-11-12 | GSE81196 | GEO

single-cell RNA-sequencing on human naïve and memory CD4+ T cells during Plasmodium falciparum infection

Project description:Plasmodium falciparum (Pf) malaria causes high rates of morbidity and mortality and lacks an effective vaccine. Clinical immunity develops in residents of malaria endemic regions which confers reduced clinical symptoms during infection and protects against severe disease. We hypothesized that understanding the immune mechanisms of clinical immunity could inform vaccine design to improve efficacy. We compared the peripheral blood cellular and humoral immune responses during Pf malaria infection between clinically susceptible and protected participants from a malaria endemic region in Malawi during a prospective 18-month longitudinal study. Participant classifications were defined by the number of recurrent clinical malaria episodes with susceptible participants having more than three while protected less than one episode during the study period. Protected participants exhibited higher immunoglobulin G (IgG) breadth and titers against Pf antigens, and greater antibody (Ab)-dependent Pf opsonization compared to susceptible participants, consistent with our classifications. Using high dimensional mass cytometry (CyTOF) and spectral flow cytometry, and single-cell transcriptomic analyses, we identified expanded memory CD4+ T cell clonotypes in the blood of protected participants undergoing malaria infection. These cells express a strong cytolytic T helper 1 effector program with transcripts encoding granzymes (A, B, H, M), granulysin, NKG7 and the ZEB2 master transcriptional regulator of terminally differentiated effector T cells. ZEB2+ memory CD4+ T cells were CD39hiTIGIThi and expressed multiple chemotactic and inhibitory receptors. Yet, their levels of several chemokine and checkpoint inhibitory receptors were reduced in protected compared to susceptible individuals. We propose that clonally expanded ZEB2+ cytolytic memory CD4+ Th1 cells could represent essential contributors to clinical immunity against Pf malaria infection.

2021-08-28 | GSE182536 | GEO

IL-27 produced during acute malaria infection regulates Plasmodium-specific memory CD4+ T cells

Project description:Malaria infection elicits both protective and pathogenic immune responses, and IL-27 is a critical cytokine that regulate effector responses during infection. Here, we identified a critical window of CD4+ T cell responses that is targeted by IL-27. Neutralization of IL-27 during acute infection with Plasmodium chabaudi expanded specific CD4+ T cells, which were maintained at high levels thereafter. In the chronic phase, Plasmodium-specific CD4+ T cells in IL-27-neutralized mice consisted mainly of CD127+KLRG1- and CD127-KLRG1+ subpopulations that displayed distinct cytokine production, proliferative capacity and are maintained in a manner independent of active infection. Single cell RNA-seq analysis revealed that these CD4+ T cell subsets formed independent clusters that express unique Th1-type genes. These IL-27-neutralized mice exhibited enhanced cellular and humoral immune responses and protection. These findings demonstrate that IL-27, which is produced during the acute phase of malaria infection, inhibits the development of unique Th1 memory precursor CD4+ T cells, suggesting potential implications for the development of vaccines and other strategic interventions.

2023-10-19 | GSE225556 | GEO

scRNA-seq + TCR-seq of mouse polyclonal CD4+ T cells during blood-stage malaria infection.

Project description:Blood-stage malaria infection induces differentiation of several effector CD4 + T subsets including Tfh and Th1 cells. The cues and microarchitectural niches required in secondary lymphoid organs for their formation were previously uncharacterised. Here we used scRNA-seq to profile CD4+ T cell transcriptomes upon malaria infection as a reference dataset for deconvolution of spatial transcriptomic data.

2024-07-08 | GSE244805 | GEO

The transcriptomic differences between Th1, Tr1, and Tneg cells in controlled human malaria infection

Project description:This study was designed to determine the differences in gene transcripts between CD4+ T helper (Th)1, Tr1, and Tneg cells during controlled human malaria infection.

2019-11-07 | GSE139990 | GEO

Expression data of human tonsilar CD4 positive T cell subsets

Project description:Type 1 regulatory T (Tr1) cells are one of the regulatory T cell subsets that are characterized by the production of high amount of IL-10 and lack of FOXP3 expression. Lymphocyte-activation gene 3 (LAG3) is a CD4 homologue molecule and we have previously reported that LAG3 is expressed on IL-10 producing regulatory T cells. However, naturally occurring Tr1 cells in human secondary lymphoid tissue have not been detected. We identified CD4+CD25-LAG3+ T cells in human tonsil. We compared mRNA expression of five CD4+ T cell subsets in tonsil using microarray analysis (CD4+CD25-LAG3+ T cells, CD4+CD25-CXCR5+PD-1+ follicular helper T cells (TFH), CD4+CD25+ T cells, CD4+CD25-LAG3-CD45RO+ cells and CD4+CD25-LAG3-CD45RO- cells). A human tonsil was obtained from a patient undergoing routine tonsillectomy, and five tonsillar CD4+ T cell subsets were sorted (each 1 x 10^5 cells). There is no biological replication.

2016-04-01 | E-GEOD-73927 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data