Ontology highlight
ABSTRACT:
PROVIDER: PRJNA178230 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR606917.fastq.gz | Fastqsanger.gz | |||
| SRR606918.fastq.gz | Fastqsanger.gz | |||
| SRR921542.fastq.gz | Fastqsanger.gz | |||
| SRR921543.fastq.gz | Fastqsanger.gz | |||
| SRR922172.fastq.gz | Fastqsanger.gz |
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Project description:CD8 T cells (TCs) expressing active STAT5 (STAT5CA) transcription factors were found to be superior to un-manipulated counterparts in their long-term persistence, capacity to infiltrate a tumor, thrive in its microenvironment and induce its regression. STAT5CA induced sustained expression of genes controlling tissue homing, cytolytic granule composition, Tc-1-associated effector molecules (GranzymeB+/IFNg+/TNFa+/CCL3+ but IL-2-) and potential for secondary responses. Sustained expression of both T-Bet and Eomes transcription factors was correlated with STAT5 binding to their corresponding genes by ChIPSeq analyses. Additionally, STAT5CA-expressing CD8 TCs demonstrated reduced IL-6R/TGFbRII expression and dampened IL-6 and TGFb1 signaling. Altogether, concerted STAT5/T-Bet/Eomes regulation controls homing, recall responses and resistance to Tc-17 polarization in CD8 TCs. TCRP1A CD8 T lymphocytes were activated by their cognate P1A Ag. After 24h, an active form of Stat5 (STAT5CA) was introduced in activated cells. Culture was continued for another 48h to induce their differentiation in effector T cells. These activated T cells were injected in congeneic hosts and recovered 70 days later from hosts' spleen and lymph nodes: TCRP1A eTC-STAT5CA.
2013-09-13 | E-GEOD-41818 | biostudies-arrayexpress
Project description:Transcriptome analyses of naive, effector and memory CD8 TCRP1A lymphocytes expressing or not an active form of the transcription factor Stat5. TCRP1A CD8 T lymphocytes were activated by their cognate Ag for 72h to induce their differentiation in effector T cells (TCRP1A eTL 72h: 4 replicates S1, S2, S3, S4). In some samples, an active form of Stat5 was introduced (TCRP1A Stat5ca eTL 72h: 2 replicates S9, S10). These 72h activated T cells were either purified and analyzed directly (samples mentioned above) or injected in congeneic hosts and recovered more than 20 days later from the host spleen and lymph nodes: TCRP1A eTL >d20: 2 replicates– S30, S32; TCRP1A Stat5ca eTL >d20: 4 replicates S11, S12, S13, S14). Naive TCRP1A CD8 T lymphocytes (TCRP1A-naive: 4 replicates S33, S34, S35, S36) are included as controls. TCRP1A CD8 T lymphocytes were activated by anti-CD3/CD28. After 24h, an active form of Stat5 was introduced in activated cells. Culture was continued for another 48h to induce their differentiation in effector T cells. These 72h activated T cells were either directly injected in congeneic hosts and recovered more than 14 days later from the host spleen and lymph nodes: T-BetKO Stat5ca >d14: 3 replicates S39, S40, S41.
2013-09-13 | E-GEOD-26945 | biostudies-arrayexpress
Project description:Transcriptome analyses of memory CDKN2A-/- CD8 T lymphocytes expressing an active form of the transcription factor Stat5. CDKN2A-/- CD8 T lymphocytes were activated by anti-CD3/CD28. After 40h, an active form of Stat5 was introduced in activated cells. Culture was continued for another 48h to induce their differentiation in effector T cells. These 88h activated T cells were injected in congeneic hosts and recovered 15 days later from the host spleen and lymph nodes: CDKN2A-/- Stat5ca -d15: 2 replicates– S46, S47. This study is a complement of the samples previously deposited under accession number GSE41819. Those two new samples are compared to previously deposited: - activated CD8 T lymphocytes transduced to express Stat5ca and transferred in congenic hosts: o S11 (GSM663446); o S12 (GSM663445); o S13 (GSM663444); o S14 (GSM663439). and - naive peripheral CD8 T lymphocytes : o S33 (GSM663441); o S34 (GSM663435); o S35 (GSM663449); o S36 (GSM663447).
2015-05-04 | E-GEOD-56154 | biostudies-arrayexpress
Project description:CD8 T cells (TCs) expressing active STAT5 (STAT5CA) transcription factors were found to be superior to un-manipulated counterparts in their long-term persistence, capacity to infiltrate a tumor, thrive in its microenvironment and induce its regression. STAT5CA induced sustained expression of genes controlling tissue homing, cytolytic granule composition, Tc-1-associated effector molecules (GranzymeB+/IFNg+/TNFa+/CCL3+ but IL-2-) and potential for secondary responses. Sustained expression of both T-Bet and Eomes transcription factors was correlated with STAT5 binding to their corresponding genes by ChIPSeq analyses. Additionally, STAT5CA-expressing CD8 TCs demonstrated reduced IL-6R/TGFbRII expression and dampened IL-6 and TGFb1 signaling. Altogether, concerted STAT5/T-Bet/Eomes regulation controls homing, recall responses and resistance to Tc-17 polarization in CD8 TCs.
2013-09-13 | GSE41818 | GEO
Project description:Transcriptome analyses of memory CDKN2A-/- CD8 T lymphocytes expressing an active form of the transcription factor Stat5.
2015-05-04 | GSE56154 | GEO
Project description:Transcriptome analyses of naive, effector and memory CD8 TCRP1A lymphocytes expressing or not an active form of the transcription factor Stat5.
2013-09-13 | GSE26945 | GEO
Project description:Cytokine-activated STAT proteins dimerize and bind to high-affinity motifs, and N-terminal domain-mediated oligomerization of dimers allows tetramer formation and binding to low-affinity tandem motifs, but the functions of dimers versus tetramers are unknown. We generated Stat5a and Stat5b double knock-in (DKI) N-domain mutant mice that form dimers but not tetramers, identified cytokine-regulated genes whose expression required STAT5 tetramers, and defined consensus motifs for dimers versus tetramers. Whereas Stat5- deficient mice exhibited perinatal lethality, DKI mice were viable, indicating that STAT5 dimers were sufficient for survival. Nevertheless, STAT5 DKI mice had fewer CD4+CD25+ T cells, NK cells, and CD8+ T cells, with impaired cytokine-induced proliferation and homeostatic proliferation of CD8+ T cells. DKI CD8+ T cell proliferation following viral infection was diminished and DKI Treg cells did not efficiently control colitis. Thus, tetramerization of STAT5 is dispensable for survival but is critical for cytokine responses and normal immune function. T cells were extracted from spleen of wt and STAT5 double knocked in mice, and treated with IL-2. The cells were collected from 0h (without treatment), 2h, 6h and 17h, and chipped on Affy mouse 430 2.0 arrays.
2012-04-24 | E-GEOD-36888 | biostudies-arrayexpress
Project description:Cytokine-activated STAT proteins dimerize and bind to high-affinity motifs, and N-terminal domain-mediated oligomerization of dimers allows tetramer formation and binding to low-affinity tandem motifs, but the functions of dimers versus tetramers are unknown. We generated Stat5a and Stat5b double knock-in (DKI) N-domain mutant mice that form dimers but not tetramers, identified cytokine-regulated genes whose expression required STAT5 tetramers, and defined consensus motifs for dimers versus tetramers. Whereas Stat5- deficient mice exhibited perinatal lethality, DKI mice were viable, indicating that STAT5 dimers were sufficient for survival. Nevertheless, STAT5 DKI mice had fewer CD4+CD25+ T cells, NK cells, and CD8+ T cells, with impaired cytokine-induced proliferation and homeostatic proliferation of CD8+ T cells. DKI CD8+ T cell proliferation following viral infection was diminished and DKI Treg cells did not efficiently control colitis. Thus, tetramerization of STAT5 is dispensable for survival but is critical for cytokine responses and normal immune function. Genome-wide mapping of STAT5A,STAT5B binding in mouse WT and DKI T cells (cultured with or without IL-2 for 1 hr) was conducted. RNA-Seq is conducted in mouse CD8+ T cells (WT and DKI, non-treated or treated with IL-2/IL-15 for 4 hr, 24 hr, 48 hr and 72 hr)
2012-04-25 | E-GEOD-36882 | biostudies-arrayexpress
Project description:Interleukin-15 (IL-15) is essential for the development and maintenance of natural killer (NK) cells. IL-15 activates STAT5 proteins, which can form dimers or tetramers. We previously found that NK cell numbers are decreased in Stat5a-Stat5b tetramer-deficient double knockin (DKI) mice, but the mechanism was not investigated. Here we show that STAT5 dimers are sufficient for NK cell development, whereas STAT5 tetramers mediate NK cell maturation and the expression of maturation-associated genes. Unlike the defective proliferation of Stat5 DKI CD8+ T cells, Stat5 DKI NK cells have normal proliferation to IL-15 but are susceptible to death upon cytokine withdrawal, with lower Bcl2 and increased active caspases. These findings underscore the importance of STAT5 tetramers in maintaining NK cell homeostasis. Moreover, defective STAT5 tetramer formation could represent a cause of NK cell immunodeficiency, and interrupting STAT5 tetramer formation might serve to control NK leukaemia.
2017-09-19 | GSE101470 | GEO
Project description:CD8 CDKN2A-/- lymphocytes expressing an active form of the transcription factor Stat5
| PRJNA242561 | ENA