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Effect of anti-CD3 antibody treatment on islet transcriptomes in the nonobese diabetic (NOD) mouse model

ABSTRACT: Effect of anti-CD3 antibody treatment on islet transcriptomes in the nonobese diabetic (NOD) mouse model

PROVIDER: PRJNA1150520 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30327700_1.fastq.gz	Fastqsanger.gz
	SRR30327700_2.fastq.gz	Fastqsanger.gz
	SRR30327701_1.fastq.gz	Fastqsanger.gz
	SRR30327701_2.fastq.gz	Fastqsanger.gz
	SRR30327702_1.fastq.gz	Fastqsanger.gz

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Effect of anti-CD3 antibody treatment on islet transcriptomes in the nonobese diabetic (NOD) mouse model

Project description:Type 1 Diabetes (T1D) is a chronic autoimmune disease resulting from T cell-mediated destruction of pancreatic beta cells. Although T cells are known to destroy beta cells, how they may impact non-lethal forms of beta cell stress that also contribute to T1D development is not known. Here, we established an intermittent treatment regimen using a validated monoclonal anti-CD3 antibody on the female nonobese diabetic (NOD) mouse model for T1D at late prediabetic stages that leads to depletion of antigen-specific T cells and improvement of glucose tolerance. We used mRNA-seq to explore transcriptomic changes in isolated pancreatic islets from mice treated with anti-CD3 antibody or IgG as a control.

2025-06-13 | GSE275350 | GEO

Proteome and (ox)PTP profile analysis of diabetic NOD mouse under single (anti-CD3) or combined (anti-CD3 + IL1RA) treatment

Project description:Type 1 diabetes (T1D) results from autoimmune destruction of β cells in the pancreas. Protein tyrosine phosphatases (PTPs) are candidate genes for T1D and play a key role in autoimmune disease development and β-cell function. Here, we assessed the global protein and individual PTP profile in the pancreas of diabetic NOD mice treated with anti-CD3 mAb and IL-1RA combination therapy. The treatment reversed hyperglycemia compared to the anti-CD3 alone control group. We observed enhanced expression of PTPN2, a T1D candidate gene, and endoplasmic reticulum (ER) chaperones in the islets from cured mice.

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Transcription profiling of pancreata, submandibular, and lacrimal glands from NOD-scid and C57Bl/6-scid mice to study the gene expression patterns of nonobese diabetic mice.

Project description:Prior to the onset of autoimmune destruction, type 1 diabetic patients and an animal model thereof, the nonobese diabetic (NOD) mouse, show morphological and functional abnormalities in target organs, which may act as inciting events for leukocyte infiltration. To better understand these abnormalities, but without the complications associated with inflammatory infiltrates, we examined genes expressed in autoimmune target tissues (pancreas, submandibular glands, and lacrimal glands) of NOD/scid mice and of autoimmune-resistant C57BL6/scid mice. Experiment Overall Design: Pancreata (6 weeks old mice), submandibular (9 and 15 weeks), and lacrimal glands (15 weeks) from individual NOD-scid and B6-scid mice were isolated for RNA extraction and hybridization on Affymetrix microarrays.

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Role of TLR7 and IFNAR1 in lacrimal gland autoimmunity in NOD mice

Project description:NOD mice spontaneously develop lacrimal gland inflammation. NOD mice that lack TLR7 or that lack IFNAR1 are protected from developing lacrimal gland inflammation. RNA sequencing studies were performed to compare gene expression profiles in lacrimal glands from wild-type (WT) vs Tlr7 knockout or Ifnar1 knockout nonobese diabetic (NOD) mice to determine disease-relevant gene and pathway profiles upregulated in WT lacrimal glands in either a TLR7- or IFNAR1-dependent manner.

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Comparison of gene expression signatures in pancreatic islets and pathogenic T lymphocytes from sublines of non-obese diabetic (NOD) mice

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Expression data from NOD-scid vs B6-scid pancreas, submandibular glands, & lacrimal glands

Project description:Prior to the onset of autoimmune destruction, type 1 diabetic patients and an animal model thereof, the nonobese diabetic (NOD) mouse, show morphological and functional abnormalities in target organs, which may act as inciting events for leukocyte infiltration. To better understand these abnormalities, but without the complications associated with inflammatory infiltrates, we examined genes expressed in autoimmune target tissues (pancreas, submandibular glands, and lacrimal glands) of NOD/scid mice and of autoimmune-resistant C57BL6/scid mice. Keywords: tissue expression, disease prone versus resistant strain comparison

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