Tfh scRNA-Seq
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE295947 | GEO | 2026/04/01
REPOSITORIES: GEO
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Project description:Comparison of transcriptome between early Tfh vs. early Th1 cells Blimp-1-YFP LCMV gp specific TCRtg Smarta cells were transferred into B6 mice, which were then infected with LCMV Armstrong. On day 3 after infection, splenocytes were stained to sort Blimp-1-YFP+IL-2Ra+ Th1 cells or Blimp-1-YFP-IL-2Ra- Tfh cells for RNAseq analysis. Contributor: LIAI RNAi center (LIAI)
2015-07-27 | E-GEOD-67334 | biostudies-arrayexpress
Project description:Comparison of chromatin accessibility between WT and tamoxifen-inducible deletion of TRAF3 (iTraf3−/−) SMARTA TFH cells during LCMV armstrong infection
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Project description:Comparison of transcriptome between WT and tamoxifen-inducible deletion of TRAF3 (iTraf3−/−) SMARTA or PbTII TFH cells during the infections by LCMV armstrong and Plasmodium yoelii, respectively.
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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:TFH and Th1 cells generated after viral or intracellular bacterial infections are critical for the control of infections and the development of immunological memories. However, the mechanisms that govern the choice of activated CD4 T cells to the two alternative fates remain unclear. Here, we found that reciprocal expression of TCF1 and Blimp1 between viral-specific TFH and Th1 cells started early after infection. TCF1 was intrinsically required for the differentiation of TFH cells. In the absence of TCF1, TFH cells failed to maintain their transcriptional and metabolic signatures, distinct from those in Th1 cells. Mechanistically, TCF1 functioned through forming negative feedback loops with IL-2 and Blimp1 signaling. Thus, we have demonstrated an essential role of TCF1 in TFH-cell differentiation. Tcf7 deficient and WT SMARTA CD4 T cells were isolated from mice 8 days after Lymphocytic Choriomeningitis Virus (LCMV) infection. TFH and Th1 cells were separated by FACS.
2015-09-18 | E-GEOD-65660 | biostudies-arrayexpress
Project description:Follicular helper T cells (TFH cells) are the prototypic helper T cell subset specialized to enable B cells to form germinal centers (GCs) and produce high-affinity antibodies. We found that expression of microRNAs (miRNAs) by T cells was essential for TFH cell differentiation. More specifically, we show that after immunization of mice with protein, the miRNA cluster miR-17~92 was critical for robust differentiation and function of TFH cells in a cell-intrinsic manner that occurred regardless of changes in proliferation. In a viral infection model, miR-17~92 restrained the expression of genes M-bM-^@M-^XinappropriateM-bM-^@M-^Y to the TFH cell subset, including the direct miR-17~92 target Rora. Removal of one Rora allele partially M-bM-^@M-^XrescuedM-bM-^@M-^Y the inappropriate gene signature in miR-17~92-deficient TFH cells. Our results identify the miR-17~92 cluster as a critical regulator of T cellM-bM-^@M-^Sdependent antibody responses, TFH cell differentiation and the fidelity of the TFH cell gene-expression program. Gene expression analysis of control versus miR-17~92 knockout (KO) LCMV-specific SMARTA TFH cells 5.5 days after viral infection.
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Project description:RNA-seq analysis of FVD–CD4+CD45.1+Ly6C–PD1+ TFH and FVD–CD4+CD45.1+Ly6C+PD1– TH1 cells sorted by flow cytometry at 7 days post-LCMV infection, sequenced via Illumina NovaSeq 6000.
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Project description:CD4 T cell help is critical for both the generation and maintenance of germinal centers, and T follicular helper (TFH) cells are the CD4 T cell subset required for this process. SAP (SH2D1A) expression in CD4 T cells is essential for germinal center development. However, SAP-deficient mice have only a moderate defect in TFH differentiation as defined by common TFH surface markers. CXCR5+ TFH cells are found within the germinal center as well as along the boundary regions of T/B cell zones. Here we show that germinal center associated T cells (GC TFH) can be identified by their co-expression of CXCR5 and the GL7 epitope, allowing for phenotypic and functional analysis of TFH and GC TFH populations. Here we show GC TFH are a functionally discrete subset of further polarized TFH cells, with enhanced B cell help capacity and a specialized ability to produce IL-4 in a TH2-independent manner. Strikingly, SAP-deficient mice have an absence of the GC TFH subset and SAP- TFH are defective in IL-4 and IL-21 production. We further demonstrate that SLAM (Slamf1, CD150), a surface receptor that utilizes SAP signaling, is specifically required for IL-4 production by GC TFH. GC TFH cells require IL-4 and IL-21 production for optimal help to B cells. These data illustrate complexities of SAP-dependent SLAM family receptor signaling, revealing a prominent role for SLAM receptor ligation in IL-4 production by germinal center CD4 T cells but not in TFH and GC TFH differentiation. Analysis of in vivo antigen-specific (LCMV-specific, SMARTA TCR transgenic) WT and Sh2d1a-/- follicular helper CD4 T cells (CXCR5high),versus non-follicular helper CD4 T cells (CXCR5low), eight days after viral infection.
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Project description:Following infection with LCMV, CD4+ SMARTA TCR transgenic cells (specific for the gp61-80 epitope of the LCMV glycoprotein) rapidly expand, become effector cells, and go on to form a long-lived memory population. Following infection with a recombinant Listeria monocytogenes expressing the LCMV epitope gp61-80, SMARTA cells also expand but display defective effector differentiation and fail to form memory. In an attempt to understand the signals required for CD4 T cell memory differentiation, we compared gene expression by SMARTA cells at the peak of the primary response following either Lm-gp61 or LCMV infection. Experiment Overall Design: SMARTA cells were purified at day 7 post-infection with either LCMV or Lm-gp61. SMARTA cells were sorted on the basis of Thy1.1 expression using a FACSAria. Cells were sorted through the machine twice to enhance purity. Two biological replicates of each group are provided. Each replicate represents the results of SMARTA pooled from three animals.
2008-06-11 | E-GEOD-10094 | biostudies-arrayexpress
Project description:Analysis of in vivo antigen-specific (LCMV-specific, SMARTA TCR transgenic) follicular helper CD4 T cells (CXCR5high),versus non-follicular helper CD4 T cells (CXCR5low), eight days after viral infection. A paper including data analysis of these experiments has been accepted for publication (Robert J. Johnston et al. Bcl6 and Blimp-1 are reciprocal and antagonistic regulators of follicular helper CD4 T cell differentiation). Experiment Overall Design: Analysis of in vivo antigen-specific (LCMV-specific, SMARTA TCR transgenic) follicular helper CD4 T cells (CXCR5high), versus non-follicular helper CD4 T cells (CXCR5low), eight days after viral infection.
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