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Acute CD8+ T cell responses to viral infection harbor Tcf1-dependent stem-like cells that quantitatively yield central memory

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE144383 | GEO | 2020/10/30

REPOSITORIES: GEO

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Acute CD8+ T cell responses to viral infection harbor Tcf1-dependent stem-like cells that quantitatively yield central memory [ATAC-seq]

Project description:Central memory CD8+ T cells (TCM) can protect from secondary pathogen infection, from chronic infection and cancer as a result of their stem cell-like properties. However, the developmental origin of central memory cells and consequently the basis of their stemness have not been resolved. By monitoring the expression of the transcription factor Tcf1 (Tcf7), which is essential for central memory formation, we identified a small subset of CD8+ T cells present during the acute response to primary infection. These cells lacked cytotoxic effector function, resembled TCM both transcriptionally and epigenetically, had stem cell-like properties, and quantitatively yielded TCM. Stemness effector phase Tcf7+ CD8+ T cells depended on Tcf1 protein expression and on a set of Tcf1-dependent genes associated with adult stem cells. Stemness was thus not acquired subsequent to antigen clearance but was maintained in rare CD8+ T cells responding to acute infection and these cells quantitatively yielded TCM.

2020-10-30 | GSE144382 | GEO

Acute CD8+ T cell responses to viral infection harbor Tcf1-dependent stem-like cells that quantitatively yield central memory [RNA-seq]

2020-10-30 | GSE142409 | GEO

Acute CD8+ T cell responses to viral infection harbor Tcf1-dependent stem-like cells that quantitatively yield central memory

Project description:Acute CD8+ T cell responses to viral infection harbor Tcf1-dependent stem-like cells that quantitatively yield central memory

| PRJNA603536 | ENA

Acute CD8+ T cell responses to viral infection harbor Tcf1-dependent stem-like cells that quantitatively yield central memory [ATAC-seq]

Project description:Acute CD8+ T cell responses to viral infection harbor Tcf1-dependent stem-like cells that quantitatively yield central memory [ATAC-seq]

| PRJNA603535 | ENA

Acute CD8+ T cell responses to viral infection harbor Tcf1-dependent stem-like cells that quantitatively yield central memory [RNA-seq]

Project description:Acute CD8+ T cell responses to viral infection harbor Tcf1-dependent stem-like cells that quantitatively yield central memory [RNA-seq]

| PRJNA596962 | ENA

Tcf1 preprograms the mobilization of glycolysis in central memory CD8<sup>+</sup> T cells during recall responses.

Project description:The mechanisms underlying the heightened protection mediated by central memory CD8+ T (TCM) cells remain unclear. Here we show that the transcription factor Tcf1 was required in resting TCM cells to generate secondary effector CD8+ T cells and to clear pathogens during recall responses. Recall stimulation of CD8+ TCM cells caused extensive reprogramming of the transcriptome and chromatin accessibility, leading to rapid induction of glycolytic enzymes, cell cycle regulators and transcriptional regulators, including Id3. This cluster of genes did not require Tcf1 in resting CD8+ TCM cells, but depended on Tcf1 for optimal induction and chromatin opening in recall-stimulated CD8+ TCM cells. Tcf1 bound extensively to these recall-induced gene loci in resting CD8+ TCM cells and mediated chromatin interactions that positioned these genes in architectural proximity with poised enhancers. Thus, Tcf1 preprogramed a transcriptional program that supported the bioenergetic and proliferative needs of CD8+ TCM cells in case of a secondary challenge.

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Differential Requirements for Tcf1 Long Isoforms in CD8+ and CD4+ T Cell Responses to Acute Viral Infection.

Project description:In response to acute viral infection, activated naive T cells give rise to effector T cells that clear the pathogen and memory T cells that persist long-term and provide heightened protection. T cell factor 1 (Tcf1) is essential for several of these differentiation processes. Tcf1 is expressed in multiple isoforms, with all isoforms sharing the same HDAC and DNA-binding domains and the long isoforms containing a unique N-terminal ?-catenin-interacting domain. In this study, we specifically ablated Tcf1 long isoforms in mice, while retaining expression of Tcf1 short isoforms. During CD8+ T cell responses, Tcf1 long isoforms were dispensable for generating cytotoxic CD8+ effector T cells and maintaining memory CD8+ T cell pool size, but they contributed to optimal maturation of central memory CD8+ T cells and their optimal secondary expansion in a recall response. In contrast, Tcf1 long isoforms were required for differentiation of T follicular helper (TFH) cells, but not TH1 effectors, elicited by viral infection. Although Tcf1 short isoforms adequately supported Bcl6 and ICOS expression in TFH cells, Tcf1 long isoforms remained important for suppressing the expression of Blimp1 and TH1-associated genes and for positively regulating Id3 to restrain germinal center TFH cell differentiation. Furthermore, formation of memory TH1 and memory TFH cells strongly depended on Tcf1 long isoforms. These data reveal that Tcf1 long and short isoforms have distinct, yet complementary, functions and may represent an evolutionarily conserved means to ensure proper programming of CD8+ and CD4+ T cell responses to viral infection.

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Programmed death 1 regulates development of central memory CD8 T cells after acute viral infection.

Project description:The T cell response possesses a number of inhibitory receptors to regulate the extent of the antiviral response and prevent immune pathology. These receptors are generally transiently upregulated during an effector response and then downregulated during memory. Some inhibitory receptors, such as programmed death 1 (PD-1) and LAG-3, were shown to be aberrantly upregulated during memory to chronic lymphocytic choriomeningitis virus infection, limiting functional capabilities. However, little is known about the impact of inhibitory receptors on memory development during a normal CD8 T cell response to acute virus infection. Our previous data showed that PD-1 is aberrantly upregulated during a secondary response by memory CD8 T cells that were generated without CD4 T cell help. Therefore, we examined the role of PD-1 in memory differentiation during acute vaccinia virus infection in intact mice. In the absence of PD-1, the primary and memory CD8 T cell responses were enhanced. Moreover, there were distinct phenotypic and functional changes in the memory PD-1(-/-) CD8 T cells. Higher levels of CD62L, CD27, and CCR7 were detected; cells produced more IL-2 and made an enhanced secondary response. These changes indicate a skewing of the memory population toward the central memory phenotype in the absence of PD-1 signaling.

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IL-10 directly suppresses CD4 but not CD8 T cell effector and memory responses following acute viral infection.

Project description:Mounting effective T cell responses is critical for eliciting long-lasting immunity following viral infection and vaccination. A multitude of inhibitory and stimulatory factors are induced following infection, and it is the compilation of these signals that quantitatively and qualitatively program the ensuing effector and memory T cell response. In response to lymphocytic choriomeningitis virus (LCMV) infection, the immunosuppressive cytokine IL-10 is rapidly up-regulated; however, how IL-10 is regulating what is often considered an "optimal" immune response is unclear. We demonstrate that IL-10 directly inhibits effector and memory CD4 T cell responses following an acutely resolved viral infection. Blockade of IL-10 enhanced the magnitude and the functional capacity of effector CD4 T cells that translated into increased and more effective memory responses. On the other hand, lack of IL-10 signaling did not impact memory CD8 T cell development. We propose that blockade of IL-10 may be an effective adjuvant to specifically enhance CD4 T cell immunity and protection following vaccination.

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Differential requirements for Tcf1 long isoforms in CD8+ and CD4+ T cell responses to acute viral infection

Project description:Comparison of the transcriptome between control Tfh and Tcf1 long isoform-deficient Tfh cells

2017-05-24 | GSE98347 | GEO