Expression profile of bcl11b-deficient cd8 T cells during immune response
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE56713 | GEO | 2014/04/12
SECONDARY ACCESSION(S): PRJNA244501
REPOSITORIES: GEO
Similar Datasets
Project description:Review on the role of Bcl11b in thymus and periphery and impact on immune diseases CD8+ T cells purified from bcl11bf/flckd-cre and wild type mice were infected with Listeria monocytogenes and on day 6 mice were sacrificed and Cd8+ T cells were purified at more than 90% purity. The RNA was purified with trizol and submitted for generation of library and microarrays to establish genes which are regulated in infected KO versus WT cytotoxic T cells.
2014-04-12 | E-GEOD-56713 | biostudies-arrayexpress
Project description:Review on the role of Bcl11b in thymus and periphery and impact on diseases
2014-04-12 | GSE56714 | GEO
Project description:Review on the role of Bcl11b in thymus and periphery and impact on diseases RNA was extracted from DP thymocytes of bcl11bf/fCd4cre/tcra-/- and tcra-/- mice. Tcra-/- mice only have preselected DP thymocytes. Such mice were used to determine the role of Bcl11b before selection, considering the defective positive selection in bcl11bf/fcd4cre mice. RNA was isolated and submitted for library generation and microarray analysis to determine expression profile of bcl11b-/- preselected DP thymocytes.
2014-04-12 | E-GEOD-56714 | biostudies-arrayexpress
Project description:Mucosal associated invariant T (MAIT) cells, already differentiated and located at mucosal sites, are critical in the body’s first wave of defenses against invading pathogens. Bcl11b KO MAIT cells fail to be maintained both in the thymus and peripheral organs. Furthermore, MAIT cells fail to fully develop in the thymus without Bcl11b, failing to upregulate RORγt, and that phenotype remains in the lungs and livers of these mice. Bcl11b deletion in MAIT cells causes dramatic shifts in the activation and TH17 programs, due to the binding of Bcl11b in many of those genes, which we have seen in the human MAIT cells. MAIT cells rely on PLZF and RORγt for their development and function, while also heavily relying on Bcl11b. These data show the key interplay of Bcl11b with PLZF and RORγt in a T cell leading to its development and necessary function to protect the body against diseases.
2021-03-22 | GSE145778 | GEO
Project description:Naïve CD44low CD25low CD8+ T cells from Bcl11bF/F/dLck-iCre and wild type mice at steady state were sorted at 90% purity, RNA was extracted and profile for mRNA expression to identify mRNAs differentially expressed in Bcl11b-/- naïve CD8+ T cells versus wild type. Naïve CD44low CD25low CD8+ T cells purified from Bcl11bF/F/dLck-iCre and wild type mice and investigated for mRNA expression
2014-04-22 | E-GEOD-56925 | biostudies-arrayexpress
Project description:Mucosal associated invariant T (MAIT) cells, already differentiated and located at mucosal sites, are critical in the body’s first wave of defenses against invading pathogens. Bcl11b KO MAIT cells fail to be maintained both in the thymus and peripheral organs. Furthermore, MAIT cells fail to fully develop in the thymus without Bcl11b, failing to upregulate RORγt, and that phenotype remains in the lungs and livers of these mice. Bcl11b deletion in MAIT cells causes dramatic shifts in the activation and TH17 programs, due to the binding of Bcl11b in many of those genes, which we have seen in the human MAIT cells. MAIT cells rely on PLZF and RORγt for their development and function, while also heavily relying on Bcl11b. These data show the key interplay of Bcl11b with PLZF and RORγt in a T cell leading to its development and necessary function to protect the body against diseases.
2021-03-22 | GSE145776 | GEO
Project description:Naïve CD44low CD25low CD8+ T cells from Bcl11bF/F/dLck-iCre and wild type mice at steady state were sorted at 90% purity, RNA was extracted and profile for mRNA expression to identify mRNAs differentially expressed in Bcl11b-/- naïve CD8+ T cells versus wild type.
2014-04-22 | GSE56925 | GEO
Project description:Transcriptional profiling of mouse iNKT cells comparing wild type and Bcl11b deficient cell. The mice were treated with 4 μg of α-galactosylceramide. Goal was to determine the effects of transcription factor Bcl11b removal in iNKT cells. Intraperitoneal treatment with 4 μg of α-Galactosylceramide. Two pair of wild type (BCL11b F/F Vα14 transgenic) and Knock out (BCL11b F/F PLZF-Cre Vα14 transgenic)) mice were treated. Lymphocytes from spleen and liver were enriched and stain with PBS-57 Loaded CD1d tetramer. Pure iNKT cells were collected through cell sorter.
2016-08-10 | E-GEOD-73679 | biostudies-arrayexpress
Project description:We recently found that a unique subset of innate-like γδ T cells develop from the DN2a-stage of the fetal thymus independent of the zinc-finger transcription factor B-cell leukemia/lymphoma 11b (Bcl11b). Herein we characterized these Bcl11b-independent γδ T cells in the periphery as CD5−NK1.1+ and Granzyme B+, and show that they are capable of producing interferon (IFN)-γ upon T cell receptor stimulation without Ca2+ influx. In wild-type mice, these cells were sparse in lymphoid tissues but abundant in non-lymphoid tissues such as the liver. Bcl11b-independent CD5−NK1.1+ γδ T cells appeared and contributed to early protection before Bcl11b-dependent CD5+NK1.1− γδT cells following Listeria monocytogenes infection, recapitulating their appearance during thymic development.
2017-10-11 | GSE89906 | GEO
Project description:T regulatory (Treg) cells have been studied in depth since their discovery for their potential use in therapies of autoimmune diseases. Treg cells have a suppression program that includes surface molecules CD25 (IL2R), cytotoxic T-lymphocyte associated protein 4 (CTLA4), and glucocorticoid-induced TNFR family (GITR) to limit aberrant and excessive inflammatory immune responses. We have shown that Bcl11b can bind to the CNS2 region in Foxp3 as well as the gene loci of those essential surface molecules for Treg suppression. Furthermore, we have identified a subset of Foxp3-independent genes in Treg cells directly regulated by Bcl11b binding. Bcl11b also directly represses expression of innate molecules such as transcription factors PU.1 and ID2 in Treg cells. Finally, we have also shown that removal of Bcl11b accelerates apoptosis in Treg cells as cleaved caspase 3 levels were significantly elevated in Bcl11b KO Treg cells when compared with WT Treg cells.
2019-08-07 | GSE120874 | GEO