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A comparison of the transcriptional profiles of DP CD24highCD44lowNK1.1-CD1d-tet+TCRa+ cells (i.e. very immature NKT cells) with those of more mature NKT cell subsets

ABSTRACT: Type 1 NKT cells play a critical role in controlling the strength and character of adaptive and innate immune responses. Their functional characteristics are distinct from conventional T cells, and are induced by a transcriptional program initiated by positive selection on CD4+CD8+ (double positive, DP) thymocytes. Here we examined transcriptional events in four immature thymic NKT cell subsets in a novel Vα14 TCR transgenic strain bearing greatly expanded numbers of CD24+CD44- NKT cells. We used a transcriptional regulatory network approach to map TCR validation to the transition from DP T to DP NKT cells, and positive selection and lineage commitment to the transition from DP NKT to CD4 NKT

ORGANISM(S): Mus musculus

PROVIDER: GSE106720 | GEO | 2021/12/15

REPOSITORIES: GEO

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Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells [RNA-seq]

Project description:T cell development is a complicatedly hierarchical process which is closely related with the chromatin activation and gene transcription. CD4+CD8+ double-positive (DP) thymocytes give rise to both conventional TCRαβ+ T cells and natural killer T cells, but they display different characteristics. Compared with conventional TCRαβ+ T cells, invariant natural killer T cells (iNKT cells) as the major population of NKT cells, are CD1d-restricted, recognize glycolipid antigens and rapidly exert effector functions after stimulation. However, the specific molecular mechanism of early iNKT cell development remain incompletely understood. Here the authors show that deletion of Chromatin assembly factor 1B (CHAF1b) remains the normal development of conventional TCRαβ+ T cell, but specifically impacts iNKT cell generation and completely impairs iNKT cell development from stage 0 with a PLZF independent way. This dysregulation is accompanied by a specific decrease in gene transcription of Vα14-Jα18, an impairment in TCR signaling and PLZF expression. Notably, ectopic expression of a transgenic Vα14-Jα18 TCR completely rescues these defects in Chaf1b-deficient iNKT cells. Moreover, cytokine secretion and anti-tumor activity are substantially maintained in Chaf1b-deficient iNKT cells with transgenic Vα14-Jα18 TCR. Our study identifies CHAF1b as a distinct regulator controls early development of iNKT cells via transcriptional regulation of Vα14-Jα18.

2021-05-21 | GSE149176 | GEO

Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells [ATAC-seq]

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RNAseq analysis of thymic CD4-CD8- double-negative (DN) invariant NKT cells from CD4+CD8+ double-positive (DP)-specific Rag2-conditional knock-out mice

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A comparison of the transcriptional profiles of DP CD24highCD44lowNK1.1-CD1d-tet+TCRa+ cells (i.e. very immature NKT cells) with those of more mature NKT cell subsets

Project description:A comparison of the transcriptional profiles of DP CD24highCD44lowNK1.1-CD1d-tet+TCRa+ cells (i.e. very immature NKT cells) with those of more mature NKT cell subsets

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Notch signaling is required for induction of an innate T cell development program in human thymus

Project description:CD4 CD8 double positive (DP) thymocytes progressively shut down Notch signaling after β-selection allowing progression of the DP program and positive selection of conventional CD4 and CD8 single positive T cells. In contrast, innate CD8+ T cells are selected from DP precursors shortly after β-selection. Here, we investigated whether notch signaling is required for the initiation of the innate T cell developmental program upon TCR engagement. We show that, after β-selection, Notch activation limits progression to late DP cells and favors the development of TCRαβ/CD3 expressing CD8dim early DP progenitors. TCR engagement in these Notch dependent TCRαβ+ early DP precursors does not induce prominent apoptosis, but rather induces T-bet expression by an mTOR-dependent mechanism. Our findings indicate that Notch signaling drives the launch of an innate effector program in response to TCR agonist selection in the thymus.

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2011-04-22 | E-GEOD-28726 | biostudies-arrayexpress

NKT, CD1d-aGC+ Va24-, and CD4 T cell clones from human peripheral blood

Project description:Microarray analysis was performed to determine the transcriptional profiles of NKT, CD1d-aGC+ Va24-, and CD4 T cells.

2011-04-22 | GSE28726 | GEO

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2012-02-06 | E-GEOD-34254 | biostudies-arrayexpress

Mature thymic NKT and T cells

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