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Gene expression data from LCMV-specific WT and Tcf7-/- follicular T helper cells

ABSTRACT: We did microarray experiments to elucidate the transcriptome changes due to TCF-1 deficiency in Tfh cells. These data clearly demonstrate that Tfh-associated genes were down-regulated in TCF-1-null Tfh cells, whereas Th1-associated signatures were up-regulated, indicating that TCF-1 initiates the Tfh fate by directly strengthening Tfh signatures while suppressing Th1-associated genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE65693 | GEO | 2015/07/24

SECONDARY ACCESSION(S): PRJNA274732

REPOSITORIES: GEO

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Gene expression data from LCMV-specific WT and Tcf7-/- follicular T helper cells

Project description:We did microarray experiments to elucidate the transcriptome changes due to TCF-1 deficiency in Tfh cells. These data clearly demonstrate that Tfh-associated genes were down-regulated in TCF-1-null Tfh cells, whereas Th1-associated signatures were up-regulated, indicating that TCF-1 initiates the Tfh fate by directly strengthening Tfh signatures while suppressing Th1-associated genes. We first sorted WT and TCF-1-null Tfh cells (2 samples per group, each sample was pooled from 4 mice) at day 8 after LCMV Armstrong infection. Then, we extracted RNA, which were subsequently sent to microarray analysis.

2015-07-24 | E-GEOD-65693 | biostudies-arrayexpress

TCF1 is required for the differentiation of T follicular helper (TFH) cells during viral infections

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

Early T-helper 1 Differentiation Is Marked by A Follicular Helper-like Transition: Differential Roles of STAT4 and T-bet

Project description:Follicular helper T (Tfh) cells comprise an important subset of helper T cells; however, their relationship with other helper lineages is incompletely understood. Herein, we show IL-12 acting via signal transducer and activator of transcription 4 (STAT4) induced both Il21 and Bcl6 genes, generating cells with features of both Tfh and Th1 cells. However, STAT4 also induced T-bet. Using ChIP-seq, we defined the genome-wide targets of T-bet and found that it repressed Bcl6 and other markers of Tfh cells, thereby attenuating the nascent Tfh-like phenotype in the late phase of Th1 specification. Finally, Tfh-like T cells were rapidly generated following Toxoplasma gondii infection in mice, but T-bet constrained Tfh cells expansion and consequent germinal center formation and antibody production. Our data argue that Tfh and Th1 share a transitional stage through the signal mediated by STAT4, which promotes both phenotypes. However, T-bet represses Tfh functionalities, promoting full Th1 differentiation. The roles of STAT4 and T-bet to determine T helper cell fate were investigated by comparing DNA binding profiles of STAT4 and T-bet in Th1 conditions. The functional outcome was further evaluated by profiling DNase hypersensitivity sites and histone epigenetic marks between WT and STAT4-deficient or T-bet-deficient T cells in Th1 conditions.

2011-12-27 | E-GEOD-33802 | biostudies-arrayexpress

TCF1 is required for the differentiation of T follicular helper (TFH) cells during viral infections

2015-09-18 | GSE65660 | GEO

Gene expression data from LCMV-specific WT and Ezh2-/- follicular T helper cells

Project description:Microarray experiments were performed to elucidate the transcriptome changes due to EZH2 deficiency in follicular T helper (TFH) cells. These data suggest TFH-lineage associated genes are down-regulated in EZH2-null TFH cells, indicating that EZH2 primes TFH differentiation by regulating canonical genes of TFH cells.

2018-12-25 | GSE110458 | GEO

Gene expression data from LCMV-specific Rictor-/- and WT follicular T helper cells

Project description:Microarray experiments were performed to elucidate the transcriptome changes due to Rictor deficiency in follicular T helper (TFH) cells. These data suggest TFH-lineage associated genes are down-regulated in Rictor-null TFH cells, indicating that Rictor primes TFH differentiation by regulating canonical genes of TFH cells.

2019-04-09 | GSE111536 | GEO

Functional and epigenetic studies reveal multistep differentiation and plasticity of in vitro and in vivo follicular T helper cells

Project description:Follicular T helper cells (Tfh) provide critical help to B cells for germinal center (GC) formation. Mutations affecting SLAM-associated Protein (SAP) prevent GC formation due to defective T-B cell interactions, yet effects on Tfh cell differentiation remain unclear. We describe the in vitro differentiation of functionally-competent “Tfh-like” cells that expressed Interleukin-21, Tfh markers, and Bcl6, and rescued GC formation in SAP-deficient hosts better than other T helper (Th) cells. SAP-deficient Tfh-like cells appeared virtually indistinguishable from wildtype, yet failed to support GCs in vivo. Interestingly, both Tfh-like and in vivo-derived Tfh cells could produce effector cytokines in response to polarizing conditions. Moreover, Th1, Th2 and Th17 cells could be reprogrammed to obtain Tfh characteristics. ChIP-Seq analyses revealed positive epigenetic markings on Tbx21, Gata3 and Rorc in Tfh-like and ex vivo Tfh cells, and Bcl6 in other Th cell populations, supporting the concept of plasticity between Tfh and other Th cells. Epigenetic modifications were evaluated in ChIP-Seq studies by profiling histone H3K4 and H3K27 trimethylation marks between Th1, Th2, Th17, Tfh-like, and CXCR5+PD-1+ sorted Tfh-like in vitro generated T helper cell populations and ex vivo derived Tfh cells.

2012-01-05 | E-GEOD-32864 | biostudies-arrayexpress

Early T-helper 1 Differentiation Is Marked by A Follicular Helper-like Transition: Differential Roles of STAT4 and T-bet

2011-12-27 | GSE33802 | GEO

Liver X receptor controls follicular helper T cell differentiation via repression of TCF-1

Project description:Liver X receptor (LXR) is a critical regulator of cholesterol homeostasis, and inhibits TCR-induced proliferation by altering intracellular sterol metabolism. However, the mechanisms by which LXR regulates helper T cell subset differentiation in vivo remains unclear. Here we demonstrate here that LXR is a crucial regulator of follicular helper T (Tfh) cells in vivo. Both mixed bone marrow chimera and antigen-specific T cell adoptive co-transfer studies show a specific increase in Tfh cells among LXRβ-deficient CD4+ T cell population in response to immunization and LCMV infection. Mechanistically LXRβ-deficient Tfh cells express increased levels of TCF-1 but comparable levels of Bcl6, CXCR5, and PD-1 in comparison with LXRβ-sufficient Tfh cells. Loss of LXRβ confers inactivation of GSK3β induced by either AKT/ERK activation or Wnt/β-catenin pathway, leading to elevated TCF-1 expression in CD4+ T cells. Conversely, ligation of LXR represses TCF-1 expression and Tfh cell differentiation in both murine and human CD4+ T cells. Treatment with an LXR agonist significantly diminishes Tfh cells and the levels of antigen-specific IgG upon immunization. These findings unveil a novel cell-intrinsic regulatory function of LXR in Tfh cell differentiation via controlling GSK3β-TCF1 pathway, which might be a promising target for pharmacological intervention in Tfh-mediated diseases.

2023-02-06 | GSE224303 | GEO

RNA-seq of CD4+ Helper T cell subsets (Th1 and Tfh) during LCMV-Armstrong infection

Project description:CD4+ memory T cells play a pivatol role in mediating long-term immunity and therefore are an important target in vaccine development. Multiple functionally distinct helper CD4+ T cell subsets can arise in response to a single invading pathogen, complicating the identification of rare memory CD4+ T cells. Here we found that expression of Id3, an inhibitor of E protein transcription factors, identified a population of cells within both the CD4+ Tfh and Th1 helper lineages that exhibited memory potential in response to secondary infection. Notably, a subset of Th1 memory cells expressing Id3 exhibited enhanced expansion upon response to pathogen, generating both Th1 and Tfh secondary effector cell populations, and displayed enrichment of key molecules associated with memory potential when compared to Id3lo Th1 cells. Thus, Id3 expression serves as an important marker of multipotent memory CD4+ T cells.

2022-07-01 | GSE175741 | GEO

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