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Control of CD8+ T cell proliferation by the transcription factor ELF4

ABSTRACT: Transcription factors that regulate quiescence, proliferation, and homing of lymphocytes are critical for effective immune system function. In the present study, we demonstrated that the transcription factor ELF4 directly activates the tumor suppressor KLF4 downstream of T cell receptor (TCR) signaling to induce cell cycle arrest in naïve CD8+ T cells. Elf4- and Klf4-deficient mice accumulated CD8+CD44hi T cells during steady-state conditions and generated more memory T cells after immunization. The homeostatic expansion of CD8+CD44hi T cells in Elf4-null mice resulted in a redistribution of cells to non-lymphoid tissue due to reduced expression of the transcription factor KLF2, and the surface proteins CCR7 and CD62L. This work describes the combinatorial role of lymphocyte-intrinsic factors in the control of T cell homeostasis, activation and homing.

ORGANISM(S): Mus musculus

PROVIDER: GSE15324 | GEO | 2009/03/24

SECONDARY ACCESSION(S): PRJNA115863

REPOSITORIES: GEO

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Transcription profiling of mouse CD8+ T cells from wild type and Elf4-/- mice left untreated or activated in vitro by culturing on anti-CD3 coated plates and anti-CD28 in media

Project description:Transcription factors that regulate quiescence, proliferation, and homing of lymphocytes are critical for effective immune system function. In the present study, we demonstrated that the transcription factor ELF4 directly activates the tumor suppressor KLF4 downstream of T cell receptor (TCR) signaling to induce cell cycle arrest in naÃ¯ve CD8+ T cells. Elf4- and Klf4-deficient mice accumulated CD8+CD44hi T cells during steady-state conditions and generated more memory T cells after immunization. The homeostatic expansion of CD8+CD44hi T cells in Elf4-null mice resulted in a redistribution of cells to non-lymphoid tissue due to reduced expression of the transcription factor KLF2, and the surface proteins CCR7 and CD62L. This work describes the combinatorial role of lymphocyte-intrinsic factors in the control of T cell homeostasis, activation and homing. Experiment Overall Design: CD8 T cells were purified from spleen of wild type and Elf4-/- mice and CD8 T cells were left untreated or activated in vitro by culturing on anti-CD3 coated plates and anti-CD28 in media (RPMI 10% FBS supplemented with 5% T-stim) for 3.5 days. Experiment Overall Design: RNAs isolated from wild type and Elf4 -/- CD8+ T cells were used in Affimetrix oligonucleotide arrays either untreated or after 3.5 days of activation.

2009-03-28 | E-GEOD-15324 | biostudies-arrayexpress

Gene expression signatures for ELF4

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Human autoinflammatory disease reveals ELF4 as a transcriptional regulator of inflammation

Project description:Transcription factors specialized to limit the destructive potential of inflammatory immune cells remain ill-defined. We discovered loss-of-function variants in the X-linked ETS transcription factor gene ELF4 in multiple unrelated male patients with early-onset mucosal autoinflammation and inflammatory bowel disease (IBD) characteristics including fevers and ulcers that responded to IL-1, TNF, or IL-12p40 blockade. Using cells from patients and two newly generated mouse models, we uncovered hyperinflammatory responses of ELF4-mutant macrophages to a range of innate stimuli. Mechanistically, Elf4 in macrophages both sustained expression of anti-inflammatory genes such as Il1rn and limited upregulation of inflammation amplifiers, including S100A8, Lcn2, Trem1, and neutrophil chemoattractants. Indeed, therapeutic Trem1 blockade reversed inflammation and intestine pathology in Elf4-mutant mice challenged with lipopolysaccharide in vivo. Thus, the ELF4 transcription factor restrains inflammation and protects against mucosal disease, a discovery with broad translational relevance for human inflammatory diseases such as IBD.

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Genome-wide screening for ELF4-binding sites.

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RNA-seq of colon tissue from wild type and Elf4-/- mice with colitis

Project description:ELF4 is a transcription factor, and to identify its potential targets, the inflamed colons of wild type and Elf4 deficient mice were subjected to whole genome RNA sequencing.

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Genome-wide screening for ELF4-binding sites.

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Gene expression signatures for ELF4

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and ELF4-/- CACO2 cells Transcriptomes

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Expression data of statin treated HUVEC cells transfected siRNA KLF2 or KLF4.

Project description:KLF2 and KLF4 are important transcriptional factors in endothelial cells, however their roles in statin treatment has not been elucidated. Here we report the comprehensive change of transcripts of statin treated HUVECs transfected with siRNA KLF2 or KLF4. We used repeated microarray analysis of HUVECs treated with pitavastatin for 4hours. Before statin treatment, cells were transfected with siRNA KLF2 or KLF4.

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