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Targeting BCL11B in chimeric antigen receptor-engineered lymphoid progenitors propagates adaptive NK-like cell responses against leukemia

ABSTRACT: Targeting BCL11B in chimeric antigen receptor-engineered lymphoid progenitors propagates adaptive NK-like cell responses against leukemia

PROVIDER: PRJNA1060768 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27411653.fastq.gz	Fastqsanger.gz
	SRR27411654.fastq.gz	Fastqsanger.gz
	SRR27411655.fastq.gz	Fastqsanger.gz
	SRR27411656.fastq.gz	Fastqsanger.gz
	SRR27411657.fastq.gz	Fastqsanger.gz

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Targeting BCL11B in chimeric antigen receptor-engineered lymphoid progenitors propagates adaptive NK-like cell responses against leukemia

Project description:Chimeric antigen receptor (CAR)-induced suppression of the transcription factor B cell CLL/lymphoma 11B propagates CAR-induced killer (CARiK) cell development. Here, we show that CRISPR-mediated BCL11B knockout (ko) in early lymphoid progenitors distinctively modulates this process depending on its use alone or in combination with a CAR. Upon adoptive transfer into hematopoietic stem cell recipients, Bcl11b-edited progenitors mediated either innate or adaptive anti-leukemic immune responses. With CAR expression being a prerequisite for antigen-specific CARiK responses, additional BCL11B ko was critical for the acquisition of adaptive killer cell functions such as clonal expansion, persistence, and recall responses. These findings have important insights on how BCL11B targeting can be used to tailor anti-leukemia functionality of CAR-engineered lymphoid progenitor cells.

2025-01-01 | GSE252499 | GEO

Chimeric Antigen Receptor-Induced Bcl11b Suppression Propagates Natural Killer-Like Cell Development

Project description:The transcription factor B Cell CLL/Lymphoma 11B (BCL11B) is indispensable for T lineage development of lymphoid progenitors. Here we show that chimeric antigen receptor (CAR) expression early in ex vivo generated lymphoid progenitors suppresses Bcl11b, leading to suppression of T cell-associated gene expression and acquisition of natural killer (NK) cell-like properties. These results give important insights into differentiation of murine and human lymphoid progenitors driven by synthetic CAR transgene-expression and inform the potential use of ex vivo generated CARiK cells as a broadly applicable product for targeted immunotherapy.

2019-12-31 | GSE135015 | GEO

Chimeric Antigen Receptor-Induced Bcl11b Suppression Propagates Natural Killer-Like Cell Development

Project description:Chimeric Antigen Receptor-Induced Bcl11b Suppression Propagates Natural Killer-Like Cell Development

| PRJNA557165 | ENA

Transcription factor Bcl11b controls identity and function of mature innate lymphoid cells type II

Project description:Type-2 innate lymphoid cells (ILC2s) promote anti-helminth responses and contribute to allergies. Though Bcl11b has been previously considered a T-lineage identity transcription factor (TF) that restrains the innate-cell genetic programs, we report here that Bcl11b is highly expressed in mature ILC2s and acts upstream of the key ILC2 TFs Gfi1, Gata-3, and of IL-33 receptor IL1rl1 (T1ST2). Additionally, Bcl11b-/- ILC2s de-repressed Rorγt, Ahr and IL-23 receptor, normally expressed in type-3 ILCs (ILC3s). Consequently, Bcl11b-/- ILC2s lost ILC2 functions and gained ILC3 functions, expanding in response to the protease allergen papain, however producing IL-17 and IL-22, and not IL-5 and IL-13, causing lung neutrophilia rather than eosinophilia, and diminished mucus production. Our results broaden Bcl11b's role from a T-cell only TF, and establishes that Bcl11b sustains mature ILC2 genetic and functional programs and lineage fidelity through positive regulation of essential ILC2 TFs and negative regulation of pivotal ILC3 TFs. RNA-seq analysis on sorted ILC2s from the mLNs of Bcl11bF/F Cre-ERT2 and wildtype mice at steady state following tamoxifen mediated deletion of Bcl11b

2015-07-28 | E-GEOD-67437 | biostudies-arrayexpress

Chimeric antigen receptor-induced BCL11B suppression propagates NK-like cell development.

Project description:The transcription factor B cell CLL/lymphoma 11B (BCL11B) is indispensable for T lineage development of lymphoid progenitors. Here, we show that chimeric antigen receptor (CAR) expression during early phases of ex vivo generation of lymphoid progenitors suppressed BCL11B, leading to suppression of T cell-associated gene expression and acquisition of NK cell-like properties. Upon adoptive transfer into hematopoietic stem cell transplant recipients, CAR-expressing lymphoid progenitors differentiated into CAR-induced killer (CARiK) cells that mediated potent antigen-directed antileukemic activity even across MHC barriers. CD28 and active immunoreceptor tyrosine-based activation motifs were critical for a functional CARiK phenotype. These results give important insights into differentiation of murine and human lymphoid progenitors driven by synthetic CAR transgene expression and encourage further evaluation of ex vivo-generated CARiK cells for targeted immunotherapy.

| S-EPMC6877334 | biostudies-literature

Cell-type specific action of Bcl11b in early T-lineage and group 2 innate lymphoid cell

Project description:The zinc finger transcription factor, Bcl11b, is expressed in T cells and group 2 innate lymphoid cells (ILC2s) among hematopoietic cells. In early T-lineage cells, Bcl11b directly binds and represses endogenous E protein antagonist, Id2, expression to prevent pro-T cell from adopting an innate-like fate. In contrast, ILC2s co-express both Bcl11b and Id2. Here, to address this contradiction, we have directly compared Bcl11b action mechanisms in pro-T cells and ILC2s. We found that Bcl11b binds to distinctive genomic regions across the genome with cell-type specific motif preferences. Bcl11b occupies functionally different sites in lineage specific way and controls totally different sets of target genes, while both of cell types use the same distal enhancer region to control timing of Bcl11b activation. In addition, Bcl11b seems to have cell-type specific post-translational modifications and to organize differential protein complexes. Therefore, despite pro-T cells and ILC2s share Bcl11b for their optimal development and function, Bcl11b is able to regulate substantially different target genes.

2019-10-19 | GSE131082 | GEO

T:B cell cooperation in ectopic lymphoid follicles propagates CNS autoimmunity

Project description:T:B cell cooperation in ectopic lymphoid follicles propagates CNS autoimmunity

| PRJNA1174079 | ENA

Transcription factor Bcl11b controls identity and function of mature innate lymphoid cells type II

2015-07-28 | GSE67437 | GEO

BCL11B

Project description:BCL11B

| PRJNA330816 | ENA

Genome-wide identification of Bcl11b gene targets

Project description:B-cell leukemia/lymphoma 11B (Bcl11b) is a transcription factor showing predominant expression in the striatum. To date, there are no known gene targets of Bcl11b in the nervous system. Here, we define targets for Bcl11b in striatal cells by performing genome-wide expression profiling. Transcriptome-wide analysis revealed that 694 genes were significantly altered in striatal cells over-expressing Bcl11b, including genes showing striatal-enriched expression similar to Bcl11b. Functional analysis on the gene target list identified significant association of Bcl11b to brain-derived neurotrophic factor/neurotrophin signaling. These data implicate Bcl11b as a novel regulator of the BDNF signaling pathway, which is disrupted in many neurological disorders. n=4 wt STHdh striatal cells and n=4 Bcl11b-transfected STHdh striatal cells

2011-08-01 | E-GEOD-31096 | biostudies-arrayexpress

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