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Role of Dec1 transcription factor in naive CD4+ T cell activation transcriptome

ABSTRACT: We used microarrays to detail the global gene transcription effect of Dec1 underlying T cells activation during the first 24 hours after stimulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE39595 | GEO | 2013/07/03

SECONDARY ACCESSION(S): PRJNA171180

REPOSITORIES: GEO

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Role of Dec1 transcription factor in naive CD4+ T cell activation transcriptome

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Project description:A transgenic mouse was generated using a CD2-driven transgene containing the cDNA of Ppp2ca to achieve over-expression of PP2Ac in T cells. NaÃ¯ve CD4 T cells were isolated and lysed at times 0, 6, and 24 hours after stimulation with anti-CD3 and anti-CD28 NaÃ¯ve CD4 T cells from wild type mice were compared with naÃ¯ve CD4 T cells from PP2Ac transgenic mice

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Naive CD4+ T cell activation transcriptome

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

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Integrated proteomic analysis of Tumor Necrosis Factor α and Interleukin 1 β-induced endothelial inflammation

Project description:Objective The vascular endothelium provides a unique interaction plane for plasma proteins and leukocytes in inflammation. It has been established that particular proteins, including ICAM1, VCAM1 and SELE, are upregulated on the endothelial cell surface in the presence of pro-inflammatory cytokines Tumor Necrosis Factor α (TNFα) and Interleukin 1β (IL-1β). We now map cytokine-induced proteomic alterations to gain further insight into endothelial inflammation. Approach and results We evaluated alterations in the in-depth proteome, cell surface proteome and phosphoproteome after 24 hours of cytokine stimulation. In addition, protein expression profiles were measured after 4, 8, 16 and 24 hours of stimulation. We found that cytokine-stimulation induced a two-step response. After 4 hours, initial protein alterations were detected, including upregulation of ICAM1 and SELE, followed by a second burst of regulation after 8 to 16 hours, which included proteins involved in antigen processing, cytokine production, virus defense and ECM-interaction. Furthermore, we found that TNFα and IL-1β provoke a highly similar endothelial response with few specific alterations. Using a novel cell surface proteomics approach, we observed highly similar changes on the cell surface. Two surface proteins displayed altered labeling of specific epitopes, suggesting that these sites are modified or involved in interactions. Combined, our integrated proteomic data describes a full array of affected processes: leukocyte interaction, self-antigen presentation, cytokine production, nitric oxide production and extracellular matrix interaction. Conclusions Our study provides a detailed quantitative proteomic analysis of endothelial inflammation in which novel inflammation-responsive proteins were uncovered, and a two-step cytokine response was identified.

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Activation of naive CD4 T cells by anti-CD3 reveals an important role for Fyn in Lck-mediated signaling.

Project description:Although there was no impairment in IL-2 secretion and proliferation of Fyn-deficient naïve CD4 cells after stimulation with antigen and antigen-presenting cells, stimulation of these cells with anti-CD3 and anti-CD28 revealed profound defects. Crosslinking of purified wild-type naïve CD4 cells with anti-CD3 activated Lck and initiated the signaling cascade downstream of Lck, including phosphorylation of ZAP-70, LAT, and PLC-gamma1; calcium flux; and dephosphorylation and nuclear translocation of the nuclear factor of activated T cells (NFAT)p. All of these signaling events were diminished severely in Fyn-deficient naïve cells activated by CD3 crosslinking. Coaggregation of CD3 and CD4 reconstituted this Lck-dependent signaling pathway in Fyn(-/-) T cells. These results suggest that when signaling of naïve T cells is restricted to the T cell antigen receptor, Fyn plays an essential role by positive regulation of Lck activity.

| S-EPMC522036 | biostudies-literature

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