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Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells [RNA-seq]

ABSTRACT: Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells [RNA-seq]

PROVIDER: PRJNA837538 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19178504_1.fastq.gz	Fastqsanger.gz
	SRR19178504_2.fastq.gz	Fastqsanger.gz
	SRR19178505_1.fastq.gz	Fastqsanger.gz
	SRR19178505_2.fastq.gz	Fastqsanger.gz
	SRR19178506_1.fastq.gz	Fastqsanger.gz

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Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells

Project description:Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells

| PRJNA839721 | ENA

Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells [iPSC scRNAseq]

Project description:IFNa is a key regulator of the dialogue between pancreatic β-cells and the immune system in early type 1 diabetes (T1D). IFNa up-regulates HLA class I expression in human β-cells fostering autoantigen presentation to the immune system. We observed by bulk and single cell RNA sequencing that exposure of human induced pluripotent-derived islet-like cells to IFNa induces expression of HLA class I and of other genes involved in antigen presentation, including the transcriptional activator NLRC5. We next evaluated the global role of NLRC5 in human insulin-producing EndoC-βH1 and human islets cells by RNA sequencing and targeted gene/protein determination. NLRC5 regulates expression of HLA class I expression and related genes and of chemokines. NLRC5 also mediates the effects of IFNa on alternative splicing, a generator of β-cell neoantigens, suggesting that it is a central mediator of the effects of IFNa on β-cells that contribute to trigger and amplify autoimmunity in T1D.

2022-09-14 | GSE203384 | GEO

Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells [RNA-seq]

2022-09-14 | GSE202852 | GEO

Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells [iPSC bulk RNAseq]

Project description:IFNa is a key regulator of the dialogue between pancreatic β-cells and the immune system in early type 1 diabetes (T1D). IFNa up-regulates HLA class I expression in human b-cells fostering autoantigen presentation to the immune system. We observed by bulk and single cell RNA sequencing that exposure of human induced pluripotent-derived islet-like cells to IFNa induces expression of HLA class I and of other genes involved in antigen presentation, including the transcriptional activator NLRC5. We next evaluated the global role of NLRC5 in human insulin-producing EndoC-bH1 and human islets cells by RNA sequencing and targeted gene/protein determination. NLRC5 regulates expression of HLA class I expression and related genes and of chemokines. NLRC5 also mediates the effects of IFNa on alternative splicing, a generator of β-cell neoantigens, suggesting that it is a central mediator of the effects of IFNa on β-cells that contribute to trigger and amplify autoimmunity in T1D.

2022-09-14 | GSE203430 | GEO

Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells [iPSC scRNAseq]

Project description:Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells [iPSC scRNAseq]

| PRJNA839716 | ENA

Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells [iPSC bulk RNAseq]

Project description:Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells [iPSC bulk RNAseq]

| PRJNA840844 | ENA

Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β cells.

Project description:IFNα is a key regulator of the dialogue between pancreatic β cells and the immune system in early type 1 diabetes (T1D). IFNα up-regulates HLA class I expression in human β cells, fostering autoantigen presentation to the immune system. We observed by bulk and single-cell RNA sequencing that exposure of human induced pluripotent-derived islet-like cells to IFNα induces expression of HLA class I and of other genes involved in antigen presentation, including the transcriptional activator NLRC5. We next evaluated the global role of NLRC5 in human insulin-producing EndoC-βH1 and human islet cells by RNA sequencing and targeted gene/protein determination. NLRC5 regulates expression of HLA class I, antigen presentation-related genes, and chemokines. NLRC5 also mediates the effects of IFNα on alternative splicing, a generator of β cell neoantigens, suggesting that it is a central player of the effects of IFNα on β cells that contribute to trigger and amplify autoimmunity in T1D.

| S-EPMC9473574 | biostudies-literature

Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells

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

2022-09-14 | GSE203385 | GEO

NLRC5 is a transcriptional regulator of MHC class I genes

Project description:NLRC5 is a member of the NLR family of proteins. The observation that NLRC5 is found in the nucleus prompted us to perform a gene array to identify putative target genes of NLRC5. We generated Jurkat T cell lines that stably express either the wild-type or mutant forms of NLRC5 harboring mutations in the nucleotide binding domain (NBD): Walker A (deficient in nucleotide binding), Walker B (deficient in nucleotide hydrolysis), and the combined Walker AB, carrying both mutations. Site-directed mutagenesis was used to create the NLRC5 NBD mutants: Walker A (K234A), Walker B (E311Q), and Walker AB (both mutations). We compared the expression profiles of Jurkat T cells expressing GFP, or the GFP-tagged wild-type, Walker A, Walker B, or Walker AB forms of NLRC5. GFP and the Walker A and Walker AB forms of NLRC5 were considered functionally inactive, while the wild-type and Walker B forms of NLRC5 were considered functionally active. These groups were used as biological replicates to assess the effect of NLRC5 activity on gene expression.

2010-07-30 | E-GEOD-22064 | biostudies-arrayexpress

Essential role of NLRC5 in cancer immune surveillance and cancer immunoediting

Project description:Background/Objectives: Downregulation of NLRC5, the transcriptional activator of MHC class-I, results in tumor immune evasion via escape from CD8+ T cell-mediated tumor control. As NLRC5 deficiency does not abrogate CD8+ T cell development, we investigated whether NLRC5-dependent antitumor immune mechanisms are required for immune surveillance. Methods: Development of 3-methylcholanthrene (MCA)-induced endogenous fibrosarcoma was studied in Nlrc5-/- mice with Nlrc5+/+ and Rag1-/- mice serving as controls. Tumors were histologically examined. Tumor cell lines established from MCA-induced tumors were evaluated for their sensitivity to immune-mediated growth control following implantation into immunocompetent C57BL/6 and immunodeficient Rag1-/- hosts. Proteomes of MCA-induced tumors were analysed by mass spectrometry followed by pathway analysis. Results: Nlrc5-/- and Rag1-/- mice showed increased propensity to develop MCA-induced tumors with elevated growth rate compared to Nlrc5+/+ mice, and displayed significantly reduced survival. Tumors from Nlrc5+/+ and Nlrc5-/- mice, but not from Rag1-/- mice, contained necrotic areas and displayed T cell infiltration. Tumors formed by Nlrc5+/+ tumor cell lines progressed unhindered in C57BL/6 hosts that reflected their immunoedited status, whereas cell lines from Nlrc5-/- and Rag1-/- tumors were efficiently controlled, indicating their non-immunoedited status. Proteomic analysis revealed enrichment of granzyme-mediated cytolytic pathway in Nlrc5+/+ tumors that were absent in Nlrc5-/- tumors, which showed enrichment of humoral and innate immune pathways. Conclusions: Our data show that NLRC5 is required for robust tumor immune surveillance and tumor immunoediting. Compensatory humoral and innate immune mechanisms activated by the loss of NLRC5 are insufficient for cancer immune surveillance and cancer immunoediting.

2025-12-19 | PXD060523 | Pride

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