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Transcriptional profiling of CD4 T cells from control mice and from mice lacking BCL6 expression in CD4+ T cells

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

ORGANISM(S): Mus musculus

PROVIDER: GSE243863 | GEO | 2024/01/24

REPOSITORIES: GEO

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Transcriptional profiling of CD4 T cells from control mice and from mice lacking BCL6 expression in CD4+ T cells 4+4

Project description:We isolated CD4+ T cells from mice vaccinated against, and challenged with, Brucella to investigate the function of CD4+ T cell intrinsic BCL6 signaling

2024-01-24 | GSE243861 | GEO

Transcriptional profiling of CD4 T cells from control mice and from mice lacking BCL6 expression in CD4+ T cells 4+2

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Transcriptional profiling of CD4 T cells from control mice and from mice lacking BCL6 expression in CD4+ T cells

Project description:Transcriptional profiling of CD4 T cells from control mice and from mice lacking BCL6 expression in CD4+ T cells

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Transcriptional profiling of CD4 T cells from control mice and from mice lacking BCL6 expression in CD4+ T cells 4+2

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Transcriptional profiling of CD4 T cells from control mice and from mice lacking BCL6 expression in CD4+ T cells 4+4

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Bcl6 controlled gene expression in naïve CD4 T cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Transcriptional profiling of intestinal CD4(+) T cells in the neonatal and adult mice.

Project description:The adult small intestine contains more than half of the body's lymphocytes in order to maintain homeostasis with the commensal microbiota. Birth marks a transition of the intestine from a sterile to an increasingly colonized environment. The data described in this article are incremented into the work published by Torow et al. titled "Active suppression of intestinal CD4(+) TCRαβ(+) T lymphocyte maturation during the postnatal period" [1]. While most of the CD4 T cells found in the adult small intestine have an activated phenotype marked by expression of helper lineage specific genes neonatal lymphocytes exhibit a naïve phenotype. Further, direct comparison of neonatal CD4 T cells from the small intestine and the gut draining mesenteric lymph node (mLN) reveals a global transcriptional 'inactivity' of the small intestinal CD4 T cells. Here, we describe in more detail the experimental design, sample preparation and analysis that were performed to obtain and interpret the microarray data. The data set is publicly available through the Gene Expression Omnibus (GEO) database with accession number GSE60515, and the analysis and interpretation of these data are included in Torow et al. [1].

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Bcl6 controlled gene expression in naïve CD4 T cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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Transcriptional profiles of intestinal APS & CD4-T cells from control, HFD-induced prediabetic and diabetic mice

Project description:This SuperSeries is composed of the SubSeries listed below.

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Transcriptional control of rapid recall by memory CD4 T cells.

Project description:Memory T cells are distinguished from naive T cells by their rapid production of effector cytokines, although mechanisms for this recall response remain undefined. In this study, we investigated transcriptional mechanisms for rapid IFN-? production by Ag-specific memory CD4 T cells. In naive CD4 T cells, IFN-? production only occurred after sustained Ag activation and was associated with high expression of the T-bet transcription factor required for Th1 differentiation and with T-bet binding to the IFN-? promoter as assessed by chromatin immunoprecipitation analysis. By contrast, immediate IFN-? production by Ag-stimulated memory CD4 T cells occurred in the absence of significant nuclear T-bet expression or T-bet engagement on the IFN-? promoter. We identified rapid induction of NF-?B transcriptional activity and increased engagement of NF-?B on the IFN-? promoter at rapid times after TCR stimulation of memory compared with naive CD4 T cells. Moreover, pharmacologic inhibition of NF-?B activity or peptide-mediated inhibition of NF-?B p50 translocation abrogated early memory T cell signaling and TCR-mediated effector function. Our results reveal a molecular mechanism for memory T cell recall through enhanced NF-?B p50 activation and promoter engagement, with important implications for memory T cell modulation in vaccines, autoimmunity, and transplantation.

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