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IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

ABSTRACT: To investigate IL-21 producing CD4 T cells, we infected IL21-VFP reporter mice with mouse polyomavirus and compared VFP+ (IL-21+) CD4 T cells to VFP- (IL-21-) CD4 T cells in the brains and spleens.

ORGANISM(S): Mus musculus

PROVIDER: GSE225462 | GEO | 2023/02/16

REPOSITORIES: GEO

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IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

Project description:To investigate the effect of interleukin (IL)-21 signaling on CD8 T cells and compare IL21-receptor deficient CD8 T cells to CD8 T cells derived from CD4 T cell deficient mice, we infected IL21-receptor knock-out mice, CD4 T cell depleted mice, and wild-type mice intracranially with Mouse Polyomavirus. We then performed gene expression profiling analysis using data obtained from RNA-seq of CD8 T cells derived from the brains of the mice at 30 day post infection.

2022-07-22 | GSE208537 | GEO

Expression data of human tonsil centroblasts (CB) cultured w/o CD40L + IL-21

Project description:CD40L and IL-21 are major contributors to the transcriptional emergency of PC identify genes in committed B cells. In order to decipher specific CD40L- and IL21-targeted genes, fresly purified human tonsil centroblasts (n=6) were cultured for 3 hours in presence or not of CD40L and IL-21 before transciptome analysis were performed.

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Precocious Interleukin 21 expression in naïve mice defines a novel stage of T-follicular helper cell development

Project description:To define early forming IL21-expressing CD4+ T cells at the transcriptional level, we performed RNAseq on FACS-purified splenic CD4+ T cells from naïve 4 wk old IL21-VFP reporter mice based on the following criteria: naïve ICOSlo/- VFP- (N); activated ICOShi VFP- cells not expressing IL21 (ACT); and activated IL21-expressing cells ICOShi VFP+ cells (ACT IL21)

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Heterogeneity of islet-infiltrating interleukin-21+ CD4 T cells in a mouse model of type 1 diabetes

Project description:Interleukin (IL)-21 is essential for type 1 diabetes (T1D) development in the NOD mouse model. IL-21-expressing CD4 T cells are present in pancreatic islets where they contribute to disease progression. However, little is known about their phenotype and differentiation states. To fill this gap, we generated a novel IL-21 reporter NOD strain to further characterize IL-21+ CD4 T cells in T1D. IL-21+ CD4 T cells accumulate in pancreatic islets and recognize β-cell antigens. Single-cell RNA sequencing revealed that most CD4 T effector cells in islets actively express IL-21 and they are highly diabetogenic despite expressing multiple inhibitory molecules, including PD-1 and LAG3. Islet IL-21+ CD4 T cells segregate into four phenotypically and transcriptionally distinct differentiation states, less differentiated early effectors, Tfh-like cells, and two Th1 subsets. Trajectory analysis predicts that early effectors differentiate into both Tfh-like and terminal Th1 cells. We further demonstrated that intrinsic IL-27 signaling controls the differentiation of islet IL-21+ CD4 T cells, contributing to their helper function. Collectively, our study reveals the heterogeneity of islet-infiltrating IL-21+ CD4 T cells and indicates that both Tfh-like and Th1 subsets continuously produce IL-21 throughout their differentiation process, highlighting the important sources of IL-21 in T1D pathogenesis.

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IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

Project description:IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

| PRJNA935745 | ENA

IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

Project description:IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

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Opposing Roles of STAT1 and STAT3 in IL-21 Function in CD4+ T cells

Project description:Interleukin-21 (IL-21) is a type 1 cytokine essential for immune cell differentiation and function. Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling. Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4+ T cells. IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4+ T cells. RNA-Seq analysis of CD4+ T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation. Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3, and interestingly, ChIP-Seq analysis showed that STAT3 binding at Tbx21 and Ifng loci was attenuated in Stat1-deficient cells. Moreover, opposing actions of STAT1 and STAT3 on IFN- expression in CD4+ T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis (LCMV) infection. Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4+ T cells from patients with autosomal dominant hyper-IgE syndrome (AD-HIES), which is caused by STAT3 deficiency. These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions.

2015-07-01 | GSE63204 | GEO

Opposing Roles of STAT1 and STAT3 in IL-21 Function in CD4+ T cells

2015-07-01 | E-GEOD-63204 | biostudies-arrayexpress

Activation of Sez-4 cell line with IL-2, IL-15 or IL-21.

Project description:In this study we compared the effects of IL-2, IL-15, and IL-21 on the gene expression, activation of cell signaling pathways, and functional properties of cells derived from the CD4+ cutaneous T-cell lymphoma (CTCL). Whereas both IL-2 and IL-15 that signal through receptors that share the common gamma chain and the beta chain modulated the expression of >1,000 genes, IL-21 that signals via the receptor also containing gamma chain up-regulated <40 genes. All three cytokines induced tyrosine phosphorylation of Jak1 and Jak3. However, only IL-2 and IL-15 strongly activated STAT5, PI3K/Akt, and MEK/ERK signaling pathways. In contrast, IL-21 selectively activated STAT3. Whereas all three cytokines protected CTCL cells from apoptosis, only IL-2 and IL-15 promoted their proliferation. The effects of the cytokine stimulation were Jak3- and Jak1-kinase dependent. These findings document the vastly different impact of IL-2 and IL-15 vs. IL-21 on malignant CD4+ T cells. They also suggest two novel therapeutic approaches to CTCL and, possibly, other CD4+ T cell lymphomas: inhibition of the Jak1/Jak3 kinase complex and, given the known strong immunostimulatory properties of IL-21 on CD8+ T, NK, and B cells, application of this cytokine to boost an immune response against malignant CD4+ T cells. Keywords: 3 replicates in each of 4 conditions

2008-02-19 | GSE8685 | GEO

Gene expression on in vitro T cells activated with IL-21

Project description:We have analyzed the effects of IL-21 signaling on T cell activation, IL-22 production and gut inflammation In this dataset we include the results of treating T cells with IL-21. Naïve CD4+ T cells (C57BL/6) were isolated, cultured in vitro +/- IL-21 and RNA was prepared

2014-03-04 | E-GEOD-55509 | biostudies-arrayexpress

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