Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Regulation of HLA II expression in acute myeloid leukemia by CIITA methylation (RNA-seq dataset)

ABSTRACT: Regulation of HLA II expression in acute myeloid leukemia by CIITA methylation (RNA-seq dataset)

PROVIDER: PRJNA631929 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11777200_1.fastq.gz	Fastqsanger.gz
	SRR11777200_2.fastq.gz	Fastqsanger.gz
	SRR11777201_1.fastq.gz	Fastqsanger.gz
	SRR11777201_2.fastq.gz	Fastqsanger.gz
	SRR11777202_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 96

Similar Datasets

Regulation of HLA II expression in acute myeloid leukemia by CIITA methylation (RNA-seq dataset)

Project description:Acute myeloid leukemia cell lines were treated with the hypomethylating agent decitabine and interferon gamma to investigate if these treatments induce HLA II gene expression. Cells carrying either control or CIITA-targeting sgRNAs were used to test the dependence of the HLA II induction on CIITA.

2020-05-13 | GSE150372 | GEO

Regulation of HLA II expression in acute myeloid leukemia by CIITA methylation (RRBS dataset)

2020-05-13 | GSE150371 | GEO

Regulation of HLA II expression in acute myeloid leukemia by CIITA methylation (RRBS dataset)

Project description:Regulation of HLA II expression in acute myeloid leukemia by CIITA methylation (RRBS dataset)

| PRJNA631928 | ENA

Regulation of HLA II expression in acute myeloid leukemia by CIITA methylation

Project description:Regulation of HLA II expression in acute myeloid leukemia by CIITA methylation

| PRJNA631922 | ENA

CIITA-transduced glioblastoma cells uncover a rich repertoire of clinically relevant tumor-associated HLA-II antigens

Project description:CD4+ T cell responses are crucial for inducing and maintaining effective anti-cancer immunity, and the identification of HLA-II cancer-specific epitopes is key to the development of potent cancer immunotherapies. In many tumor types, and especially in glioblastoma (GBM), HLA-II complexes are hardly ever naturally expressed. Hence, little is known about immunogenic HLA-II epitopes in GBM. With stable expression of CIITA coupled to a detailed and sensitive mass spectrometry based immunopeptidomics analysis, we here uncovered a remarkable breadth of the HLA-ligandome in HROG02, HROG17 and RA GBM cell lines. The effect of CIITA expression on the induction of the HLA-II presentation machinery was striking in each of the three cell lines, and it was significantly higher compared to IFNɣ treatment. In total, we identified 16,123 unique HLA-I peptides and 32,690 unique HLA-II peptides. In order to genuinely define the identified peptides as true HLA ligands, we carefully characterized their association with the different HLA allotypes. In addition, we identified 138 and 279 HLA-I and HLA-II ligands, respectively, most of which are novel in GBM, derived from known GBM-associated tumor-antigens that have been used as source proteins for a variety of GBM vaccines. Our data further indicate that CIITA-expressing GBM cells acquired an antigen presenting cell-like phenotype as we found that they directly present external proteins as HLA-II ligands. Not only that CIITA-expressing GBM cells are attractive models for antigen discovery endeavors, but such engineered cells have great therapeutic potential through massive presentation of a diverse antigenic repertoire.

2021-02-03 | PXD020079 | Pride

CIITA

Project description:CIITA

| PRJEB5958 | ENA

Regulation of HLA II expression in acute myeloid leukemia by CIITA methylation

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-05-13 | GSE150374 | GEO

Cohesin mutations suppress HLA class II gene expression to promote immune evasion during the progression to acute leukemia in children with Down syndrome. [CRISPR]

Project description:Children with Down syndrome have a 150-fold increased risk of developing the myeloid leukemia of Down syndrome (ML-DS). ML-DS is preceded by transient abnormal myelopoiesis (TAM), which spontaneously resolves in most cases but progresses to AML with additional mutations most commonly in the cohesin complex or signaling genes. However, the mechanisms by which these alterations promote leukemia are unknown. Here, we leveraged isogenic cell lines and patient data to investigate the role of cohesin mutations in leukemia progression. Multi-omic analyses revealed that haploinsufficiency of the cohesin complex suppresses the occupancy of CIITA at HLA class II loci, leading to a reduction in HLA Class II gene expression. Surface levels of HLA-DR are lower in ML-DS relative to TAM and these decreased levels are associated with an increased risk of TAM progression. Of note, a decrease in HLA-Class II gene expression is also a feature of non-DS AML with reduced expression of cohesin family members. These data suggest that unlike TAM, ML-DS blasts may evade the immune system by reduced HLA class II expression, providing a new model for leukemia progression in DS.

2026-07-20 | GSE314927 | GEO

Cohesin mutations suppress HLA class II gene expression to promote immune evasion during the progression to acute leukemia in children with Down syndrome [CUT&Run]

2026-07-20 | GSE314930 | GEO

Cohesin mutations suppress HLA class II gene expression to promote immune evasion during the progression to acute leukemia in children with Down syndrome [ChIP-seq]

2026-07-20 | GSE314929 | GEO