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The MHC class II transactivator Ciita has a highly restricted transcriptional footprint in murine classical dendritic cells

ABSTRACT: Ciita has been suggested to control the expression of a number of genes based on ChIP-Seq or reporter anaysis but in vivo regulation beyong MHC class II has largely not been confirmed. We crossed Ciita knock out mice to Zbtb46 GFP knock-in knock out mice to identify classical dendritic cells in vivo in a Ciita deficient background. Expression microarray analysis of CD24+ and CD172a+ DCs from homeostatic spleen or activated BM Flt3l cultures show a highly resitrcited transcriptional footprint of Ciita. These findings underscore the fact that canonical binding sites active in transient expression assays may not always be functional in vivo. In addition, ChIP-Seq alone is not sufficient to discriminate binding from control of expression of a nearby gene.

ORGANISM(S): Mus musculus

PROVIDER: GSE96584 | GEO | 2018/02/16

REPOSITORIES: GEO

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CIITA

Project description:CIITA

| PRJEB5958 | ENA

CIITA

Project description:Creation of comprehensive CIITA and RFX5 ChIP-Seq profiles in primary B cells and monocytes

2014-10-08 | E-MTAB-2424 | biostudies-arrayexpress

CIITA regulated genes in human B cells

Project description:The MHC class II transactivator (CIITA) is essential for the expression of MHC-II genes. CIITA functions as a transcriptional activator when bound to genes although repressive roles have been reported at some loci in other cell types. To define the role of CIITA in gene regulation in human B cells, we performed ChIP-seq for CIITA using three independent antibodies, the histone marks H3K4me3 and H3K27ac, and ATAC-seq in the Raji human B cell line. Additionally, we profiled H3K27ac and ATAC-seq in the CIITA-null RJ2.2.5 cell line. A core set of CIITA peaks were identified that overlapped in all antibodies. Using the H3K27ac, H3K4me3, and ATAC-seq profiles generated in CIITA+ Raji and CIITA-null RJ2.2.5 cells CIITA dependent chromatin modifications were identified. These data define the CIITA regulated genes in human B cells.

2015-03-06 | GSE52941 | GEO

RNAseq analysis of U2OS cell clones made to stably expressing exogenous CIITA

Project description:Bulk RNAseq analysis was done on single cell clones of U2OS cells either expressing exogeonous CIITA or an empty vector control to identify genes regulated by CIITA expression.

2020-09-16 | GSE155204 | GEO

Osteocyte CIITA Aggravates Osteolytic Bone Lesions in Myeloma

Project description:Osteolytic destruction is a hallmark of multiple myeloma, resulting from activation of osteoclast mediated bone resorption and reduction of osteoblast-mediated bone formation. However, the molecular mechanism underlying the differentiation and activity of osteoclasts and osteoblasts within a myelomatous microenvironment remains unclear. Here, we demonstrate that the osteocyte-expressed major histocompatibility complex class II transactivator (CIITA) contributes to myeloma-induced bone lesions. CIITA upregulates the secretion of osteolytic cytokines from osteocytes through acetylation at histone 3 lysine 14 in the promoter of TNFSF11 (encoding RANKL) and SOST (encoding sclerostin), leading to enhanced osteoclastogenesis and decreased osteoblastogenesis. In turn, myeloma cell–secreted 2-deoxy-D-ribose, the product of thymidine catalyzed by the function of thymidine phosphorylase, upregulates CIITA expression in osteocytes through the STAT1/IRF1 signaling pathway. Our work thus broadens the understanding of myeloma-induced osteolysis and indicates a potential strategy for disrupting tumor-osteocyte interaction to prevent, or treat patients with, myeloma bone disease.

2022-04-23 | GSE200987 | GEO

Class II transactivator (CIITA) enhances cytoplasmic processing of HIV-1 Pr55Gag.

Project description:BackgroundThe Pr55(gag) (Gag) polyprotein of HIV serves as a scaffold for virion assembly and is thus essential for progeny virion budding and maturation. Gag localizes to the plasma membrane (PM) and membranes of late endosomes, allowing for release of infectious virus directly from the cell membrane and/or upon exocytosis. The host factors involved in Gag trafficking to these sites are largely unknown. Upon activation, CD4+ T cells, the primary target of HIV infection, express the class II transcriptional activator (CIITA) and therefore the MHC class II isotype, HLA-DR. Similar to Gag, HLA-DR localizes to the PM and at the membranes of endosomes and specialized vesicular MHC class II compartments (MIICs). In HIV producer cells, transient HLA-DR expression induces intracellular Gag accumulation and impairs virus release.Methodology/principal findingsHere we demonstrate that both stable and transient expression of CIITA in HIV producer cells does not induce HLA-DR-associated intracellular retention of Gag, but does increase the infectivity of virions. However, neither of these phenomena is due to recapitulation of the class II antigen presentation pathway or CIITA-mediated transcriptional activation of virus genes. Interestingly, we demonstrate that CIITA, apart from its transcriptional effects, acts cytoplasmically to enhance Pr160(gag-pol) (Gag-Pol) levels and thereby the viral protease and Gag processing, accounting for the increased infectivity of virions from CIITA-expressing cells.Conclusions/significanceThis study demonstrates that CIITA enhances HIV Gag processing, and provides the first evidence of a novel, post-transcriptional, cytoplasmic function for a well-known transactivator.

| S-EPMC2892040 | biostudies-literature

Gene expression profiling of Hodgkin lymphoma cell line KMH2: Comparison of CIITA-BX648577 knockdown cultures with non-silencing controls

Project description:Description of differentially expressed genes between KMH2 CIITA-BX648577 knockdown cultures and non-silencing controls To determine the change in gene expression after siRNA interference with the fusion transcript CIITA-BX 648577 identified in KMH2 cells.

2010-12-11 | E-GEOD-25987 | biostudies-arrayexpress

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

MHC class II transactivator CIITA is a recurrent gene fusion partner in lymphoid cancers.

Project description:Chromosomal translocations are critically involved in the molecular pathogenesis of B-cell lymphomas, and highly recurrent and specific rearrangements have defined distinct molecular subtypes linked to unique clinicopathological features. In contrast, several well-characterized lymphoma entities still lack disease-defining translocation events. To identify novel fusion transcripts resulting from translocations, we investigated two Hodgkin lymphoma cell lines by whole-transcriptome paired-end sequencing (RNA-seq). Here we show a highly expressed gene fusion involving the major histocompatibility complex (MHC) class II transactivator CIITA (MHC2TA) in KM-H2 cells. In a subsequent evaluation of 263 B-cell lymphomas, we also demonstrate that genomic CIITA breaks are highly recurrent in primary mediastinal B-cell lymphoma (38%) and classical Hodgkin lymphoma (cHL) (15%). Furthermore, we find that CIITA is a promiscuous partner of various in-frame gene fusions, and we report that CIITA gene alterations impact survival in primary mediastinal B-cell lymphoma (PMBCL). As functional consequences of CIITA gene fusions, we identify downregulation of surface HLA class II expression and overexpression of ligands of the receptor molecule programmed cell death 1 (CD274/PDL1 and CD273/PDL2). These receptor-ligand interactions have been shown to impact anti-tumour immune responses in several cancers, whereas decreased MHC class II expression has been linked to reduced tumour cell immunogenicity. Thus, our findings suggest that recurrent rearrangements of CIITA may represent a novel genetic mechanism underlying tumour-microenvironment interactions across a spectrum of lymphoid cancers.

| S-EPMC3902849 | biostudies-literature

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

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