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ATAC-seq and mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE119734 | GEO | 2021/07/21

REPOSITORIES: GEO

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mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

Project description:Above primary T cell subsets were isolated by magnetic isolation (including GM-CSF capture and secretion assay) from peripheral blood of 5 to 6 human healthy donors. Total RNA (and genomic DNA for an accompanying dataset) was extracted for transcriptome analysis. By integration of RNA-seq data with corresponding ATAC-seq data we generated a novel gene regulatory network of human GM-CSF producing and memory T helper cells.

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mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

Project description:mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

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ATAC-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

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ATAC-seq and mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

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Producing GM-CSF: a unique T helper subset?

Project description:GM-CSF-producing helper T cells have previously been identified to serve a nonredundant function in the initiation of autoimmune inflammation. An article by Sheng et al. recently published by Cell Research now suggests that the differentiation program of GM-CSF-producing cells from naïve CD4 T cells is distinct from that of Th1 and Th17 cells, and is regulated by the IL-7-STAT5 axis.

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CD4 T cells play important roles in maintaining IL-17-producing ?? T-cell subsets in naive animals.

Project description:A proportional balance between ?? and ?? T-cell subsets in the periphery is exceedingly well maintained by a homeostatic mechanism. However, a cellular mechanism underlying the regulation remains undefined. We recently reported that a subset of developing ?? T cells spontaneously acquires interleukin (IL)-17-producing capacity even within naive animals through a transforming growth factor (TGF)?1-dependent mechanism, thus considered 'innate' IL-17-producing cells. Here, we report that ?? T cells generated within ?? T cell (or CD4 T cell)-deficient environments displayed altered cytokine profiles; particularly, 'innate' IL-17 expression was significantly impaired compared with those in wild-type mice. Impaired IL-17 production in ?? T cells was directly related to CD4 T-cell deficiency, because depletion of CD4 T cells in wild-type mice diminished and adoptive CD4 T-cell transfer into T-cell receptor ?-/- mice restored IL-17 expression in ?? T cells. CD4 T cell-mediated IL-17 expression required TGF?1. Moreover, Th17 but not Th1 or Th2 effector CD4 T cells were highly efficient in enhancing ?? T-cell IL-17 expression. Taken together, our results highlight a novel CD4 T cell-dependent mechanism that shapes the generation of IL-17+ ?? T cells in naive settings.

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Project description:Viral compartmentalization between naïve and memory CD4(+) T cell subsets has been described, but only for individuals who were receiving antiretroviral therapy (ART). We present here an extensive analysis of the viral quasispecies residing in the naïve, central and effector memory CD4(+) T cell subsets in a number of therapy naïve individuals and representing an array of HIV-1 subtypes. We longitudinally analyzed subset-specific infection and evolution in a subtype B infected individual who switches from CCR5 to dual CCR5/CXCR4 coreceptor usage. We show that the central memory subset, the predominantly infected subset, harbors a more diverse viral population compared to the others. Through sequence analysis of the env C2V3 region we demonstrate a lack of viral compartmentalization among all subsets. Upon coreceptor switch we observe a pronounced increase in the infection level of the naïve population. Our findings emphasize the importance of all CD4(+) T cell subsets to viral evolution.

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Project description:The threat of bioterrorism with smallpox and the broad use of vaccinia vectors for other vaccines have led to the resurgence in the study of vaccinia immunological memory. The importance of the role of CD4+ T cells in the control of vaccinia infection is well known. However, more CD8+ than CD4+ T cell epitopes recognized by human subjects immunized with vaccinia virus have been reported. This could be, in part, due to the fact that most of the studies that have identified human CD4+ specific protein-derived fragments or peptides have used IFN-? production to evaluate vaccinia specific T cell responses. Based on these findings, we reasoned that analyzing a large panel of cytokines would permit us to generate a more complete analysis of the CD4 T cell responses. The results presented provide clear evidence that TNF-? is an excellent readout of vaccinia specificity and that other cytokines such as GM-CSF can be used to evaluate the reactivity of CD4+ T cells in response to vaccinia antigens. Furthermore, using these cytokines as readout of vaccinia specificity, we present the identification of novel peptides from immunoprevalent vaccinia proteins recognized by CD4+ T cells derived from smallpox vaccinated human subjects. In conclusion, we describe a "T cell-driven" methodology that can be implemented to determine the specificity of the T cell response upon vaccination or infection. Together, the single pathogen in vitro stimulation, the selection of CD4+ T cells specific to the pathogen by limiting dilution, the evaluation of pathogen specificity by detecting multiple cytokines, and the screening of the clones with synthetic combinatorial libraries, constitutes a novel and valuable approach for the elucidation of human CD4+ T cell specificity in response to large pathogens.

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Antigen-specific memory and naive CD4+ T cells following secondary Chlamydia trachomatis infection.

Project description:Memory antigen-specific CD4+ T cells against Chlamydia trachomatis are necessary for protection against secondary genital tract infection. While it is known that naïve antigen-specific CD4+ T cells can traffic to the genital tract in an antigen-specific manner, these T cells are not protective during primary infection. Here, we sought to compare the differences between memory and naïve antigen-specific CD4+ T cells in the same mouse following secondary infection using transgenic CD4+ T cells (NR1 T cells). Using RNA sequencing, we found that there were subtle but distinct differences between these two T cell populations. Naïve NR1 T cells significantly upregulated cell cycle genes and were more proliferative than memory NR1 T cells in the draining lymph node. In contrast, memory NR1 T cells were more activated than naïve NR1 T cells and were enriched in the genital tract. Together, our data provide insight into the differences between memory and naïve antigen-specific CD4+ T cells during C. trachomatis infection.

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