E-MTAB-5338
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ABSTRACT:
PROVIDER: E-MTAB-5338 | ExpressionAtlas | 2019-05-14
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:RNAseq analysis of CD4 and CD8 T cells in response to vaccinia virus infection
| PRJEB18572 | ENA
Project description:Miao2010 - Innate and adaptive immune
responses to primary Influenza A Virus infection
This model is described in the article:
Quantifying the early immune
response and adaptive immune response kinetics in mice infected
with influenza A virus.
Miao H, Hollenbaugh JA, Zand MS,
Holden-Wiltse J, Mosmann TR, Perelson AS, Wu H, Topham DJ.
J. Virol. 2010 Jul; 84(13):
6687-6698
Abstract:
Seasonal and pandemic influenza A virus (IAV) continues to
be a public health threat. However, we lack a detailed and
quantitative understanding of the immune response kinetics to
IAV infection and which biological parameters most strongly
influence infection outcomes. To address these issues, we use
modeling approaches combined with experimental data to
quantitatively investigate the innate and adaptive immune
responses to primary IAV infection. Mathematical models were
developed to describe the dynamic interactions between target
(epithelial) cells, influenza virus, cytotoxic T lymphocytes
(CTLs), and virus-specific IgG and IgM. IAV and immune kinetic
parameters were estimated by fitting models to a large data set
obtained from primary H3N2 IAV infection of 340 mice. Prior to
a detectable virus-specific immune response (before day 5), the
estimated half-life of infected epithelial cells is
approximately 1.2 days, and the half-life of free infectious
IAV is approximately 4 h. During the adaptive immune response
(after day 5), the average half-life of infected epithelial
cells is approximately 0.5 days, and the average half-life of
free infectious virus is approximately 1.8 min. During the
adaptive phase, model fitting confirms that CD8(+) CTLs are
crucial for limiting infected cells, while virus-specific IgM
regulates free IAV levels. This may imply that CD4 T cells and
class-switched IgG antibodies are more relevant for generating
IAV-specific memory and preventing future infection via a more
rapid secondary immune response. Also, simulation studies were
performed to understand the relative contributions of
biological parameters to IAV clearance. This study provides a
basis to better understand and predict influenza virus
immunity.
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2021-10-05 | BIOMD0000000546 | BioModels
Project description:Although extensive studies have demonstrated the gene expression patterns of antigen-specific CD4+ and CD8+ T-cells during chronic hepatitis C virus (HCV) infection, the transcriptional profiles of global CD4+ and CD8+ T-cells remains unclear. In this report, we recruited 10 long-term (~20 years) treatment-naM-CM-/ve chronic HCV (CHC) patients and 5 healthy donors (HDs) to investigate differences in global CD4+ and CD8+ T-cells gene expression profile. Global CD4+ and CD8+ T-cells showed unique transcriptional profiles in the expression of apoptosis-related genes. We identified BCL2, PMAIP1, and CASP1 in CD4+ T-cells and IER3 and BCL2A1 in CD8+ T-cells from CHC patients as HCV-specific gene signatures. The unique apoptosis-related gene expression profilesin global CD4+ and CD8+ T-cells programmed by chronic HCV infection seemed to enhance activation-induced apoptosis, which was suffered by global CD4+ and CD8+ T-cells. We obtained 15 blood samples to identify the gene expression signatures of global CD4+ and CD8+ T-cells due to chronic HCV infection. The samples included: 5 samples from high HCV viral load patients (HCV-h), 5 samples from low HCV viral load (HCV-l) and 5 samples from healthy donors (HD). HCV patients were all Ab+ and treatment-naive prior to the study. Samples were taken once from each individual. Global CD4+ and CD8+ T-cells were enriched by microbeads, and total RNA were used in gene chip analysis.
2013-08-19 | E-GEOD-49954 | biostudies-arrayexpress
Project description:CD4+ T cells play a critical role in sustaining the effector function of CD8+ T cells during chronic viral infection. When CD4+ T cell “help” is absent, CD8+ T cells enter a dysfunctional state, losing their capacity for viral control. However, when CD4+ T cell help is present, a heterogenous population of virus-specific CD8+ T cells are present. Here, we applied scRNA-seq to distinguish CD8+ T cell heterogeneity during LCMV Clone 13 infection.
2022-11-29 | GSE201195 | GEO
Project description:Inhibition of IFN-I signaling promotes the control of persistent virus infection, but the underlying mechanisms remain poorly understood. Here we report that genetic ablation of IFNAR1 specifically in NK cells led to elevated numbers of T follicular helper cells, germinal center B cells, and plasma cells, resulting in hastened virus clearance comparable to IFNAR1 blockade by an IFNAR1 neutralizing antibody. Antigen-specific B cells and antiviral antibodies were essential for the accelerated control of LCMV Cl13 infection following IFNAR1 blockade. IFNAR1 signaling in NK cells promoted NK cell maturation, function, and killing of antigenspecific CD4 and CD8 T cells. Therefore, Inhibition of IFN I signaling in NK cells enhances CD4 and CD8 T cell responses, elevates humoral immune response, and thereby facilitates the control of persistent virus infection.
2021-03-30 | GSE147330 | GEO
Project description:CD4 and CD8 T cells display functional defects during chronic infection such as loss of certain cytokines. Recent studies have suggested that CD4 T cells may actually gain other functions, however. Here, we analyzed gene expression profiles from LCMV-specific CD4 and CD8 T cells throughout the response to either acute LCMV or chronic LCMV infection. This alllowed us to identify CD4-specific changes during chronic infection compared to acute infection but also revealed shared core regulators between CD4 and CD8 T cells. LCMV-specific CD4 and CD8 T cells were isolated 6, 8, 15 and 30 days post infection with LCMV Armstrong or LCMV clone 13. Naïve CD4 and CD8 T cells were also isolated from naïve mice as comparisons. Four replicates of each sample were hybridized. The only exception is LCMV-specific CD4 T cells isolated 6 days post infection with LCMV-Arm where only three replicates were hybridized.
2012-12-12 | E-GEOD-30431 | biostudies-arrayexpress
Project description:Cytotoxic CD4 T lymphocytes (CD4-CTL) are important in anti-viral immunity. For example, we have previously shown that in mice, CD4-CTL are important to control ectromelia virus (ECTV) infection. How viral infections induce CD4-CTL responses remains incompletely understood. Here we demonstrate that not only ECTV but also vaccinia virus and Lymphocytic Choriomeningitis virus induce CD4-CTL, but that the response to ECTV is stronger. Using ECTV, we also demonstrate that in contrast to CD8-CTL, CD4-CTL differentiation requires constant virus replication and ceases once the virus is controlled. We also show that Major Histocompatibility Complex Class II molecules on CD11c+ cells are required for CD4-CTL differentiation and for mousepox resistance. Transcriptional analysis indicated that anti-viral CD4-CTL and non-cytolytic T Helper 1 (Th1) CD4 T cells have similar transcriptional profiles, suggesting that CD4-CTL are terminally differentiated classical Th1 cells. Interestingly, CD4-CTL and classical Th1 cells expressed similar mRNA levels of the transcription factors ThPOK and GATA-3, necessary for CD4 T cell linage commitment; and Runx3, required for CD8 T cell development and effector function. However, at the protein level, CD4-CTL had higher levels of the three transcription factors suggesting that further post-transcriptional regulation is required for CD4-CTL differentiation. Finally, using CRISPR-Cas9 deletion of Runx3 in CD4 T cells, we demonstrate that the development of CD4-CTL but not of classical Th1 CD4 T cells requires Runx3 following ECTV infection. These results further our understanding of the mechanisms of CD4-CTL differentiation during viral infection and the role of post-transcriptionally regulated Runx3 in this process.
2021-07-06 | GSE179289 | GEO
Project description:Viruses often establish persistent infections by interrupting immune cell responses. Sphingosine kinase 2 (SphK2) generates sphingosine 1-phsophate, which is known to regulate versatile cellular processes, including immune responses. However, little is known about the role of SphK2 in the immune response to viral infections. Here, we demonstrate that during lymphocytic choriomeningitis virus (LCMV) clone 13 infection, a virus known to establish a persistent infection in mice, SphK2 functions to limit CD4+ T cell responses, which aids in the establishment of virus-induced immunosuppression and viral persistence. The infection of SphK2-deficient (Sphk2-/-) mice with LCMV resulted in kidney disease and ultimately mortality. Following infection, Sphk2-/- mice were shown to have increased LCMV-specific CD4+ and CD8+ T cell responses. With the use of LCMV epitope-specific TCR transgenic mouse lines in adoptive transfer studies, SphK2 was shown to have intrinsic negative function in CD4+ T cells, but not CD8+ T cells. Furthermore, Sphk2-/- CD4+ T cells were able to promote endogenous, virus-specific CD8+ T cell responses more efficiently than Sphk2+/+ CD4+ T cells. Our results suggest that SphK2 is a novel regulator of the immune response during LCMV clone 13 infection and targeting SphK2 may provide a promising immunotherapeutic strategy for the control of persistent viral infections. This study incorporated the use of RNA sequencing to determine what pathways SphK2 was involved in to affect CD4+ T cell activity and proliferation. Sphk2+/+ or Sphk2-/- LCMV epitope-recognizing tg CD4+ T cells were transferred into C57BL/6 mice and recovered 7 days following LCMV Cl 13 infection. RNA sequencing revealed several pathways upregulated in Sphk2-/- CD4+ T cells relating to cell cycle progression, regulation of transcription, and regulation of nucleic acid binding.
2020-10-29 | GSE155030 | GEO
Project description:Title: Gene Expression analysis of naive CD8+ T-cell differentiation during a primary immune response Description: C57BL/6 wild type mice are administered GK1.5 (depleting anti CD4 antibody) or isotope control by intraperitoneal injection at 3 and 1 day pre-infection, then every 36-48 hour post infection. 24 hours pre-infection, splenocytes from F5 RAG -/- mice are stained with CFSE and 10^7 splenocytes are transfered to recipient C57BL/6 mice by intravenous injection. 24 hours laters, recipient mice are infected with 10^7 PFU of a recombinant Vaccinia virus expressing NP366-74. At timepoints 0, 12, 24, 48, 72 and 96 splenocytes are obtained and FACS sorted to obtain CD8+ T-cells.
2005-09-29 | E-MIMR-38 | biostudies-arrayexpress
Project description:Gene expression of memory CD4+ and CD8+ T cells determined by RNAseq 30 days after LCMV Armstrong infection
2019-01-08 | GSE116519 | GEO