Expression profile of bcl11b-/- preselected DP thymocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE56714 | GEO | 2014/04/12
SECONDARY ACCESSION(S): PRJNA244500
REPOSITORIES: GEO
Similar Datasets
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:Review on the role of Bcl11b in thymus and periphery and impact on immune diseases
2014-04-12 | GSE56713 | GEO
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:T-cell receptor (TCR) signals play a critical role in guiding selected thymocytes to distinct lineages by activating genes for transcription factors, such as ThPOK and Runx3, for the helper- or cytotoxic-lineage, respectively. Here we show that Bcl11b, known as an early T-lineage commitment factor, is essential for proper expression of ThPOK and Runx3. Loss of Bcl11b resulted in premature and random expression of these specification factors, leading to lineage scrambling that was disconnected from TCR restriction by MHC. Early Thpok repression by Bcl11b is independent of its known transcriptional silencer, but requires the C-terminal zinc-finger of Bcl11b. Collectively, our findings shed new light on the role of Bcl11b in priming lineage-specifying genes to integrate TCR signals into a subsequent developmental program that dissects effector lineages.
2017-07-20 | GSE90989 | GEO
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:Bcl11b hypomorphic mutant thymocytes
| PRJNA356604 | ENA
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: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-cell receptor (TCR) signals play a critical role in guiding selected thymocytes to distinct lineages by activating genes for transcription factors, such as ThPOK and Runx3, for the helper- or cytotoxic-lineage, respectively. Here we show that Bcl11b, known as an early T-lineage commitment factor, is essential for proper expression of ThPOK and Runx3. Loss of Bcl11b resulted in premature and random expression of these specification factors, leading to lineage scrambling that was disconnected from TCR restriction by MHC. Early Thpok repression by Bcl11b is independent of its known transcriptional silencer, but requires the C-terminal zinc-finger of Bcl11b. Collectively, our findings shed new light on the role of Bcl11b in priming lineage-specifying genes to integrate TCR signals into a subsequent developmental program that dissects effector lineages.
2017-07-20 | GSE90949 | GEO
Project description:Comparison of transcriptome between wild type, CD4 cre conditional knock-out and Bcl11b mutant mice.
2017-07-20 | GSE90134 | GEO