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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

Analysis of graft-infiltrating CD8+ T cell profile after CD3 antibody therapy

Project description:We performed a global gene expression analysis comparing intragraft tolerant CD8+ T cells from CD3 antibody-treated mice showing permanent islet graft survival to intra-graft effector CD8+ T cells isolated from untreated mice showing acute rejection of islet allografts. The objective was to emphasize the anergic profile of CD8+ T cells residing within the pancreatic islet allograft of mice rendered tolerant following CD3 antibody therapy.

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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.

2022-11-10 | PXD025394 | Pride

IFN-alpha induced gene expression profile in NOD/BDC2.5 and NOD mice.

Project description:With the goal of identifying changes in gene expression in CD4(+) T cells during the development of diabetes in the nonobese diabetic (NOD) mouse, we used DNA microarrays to analyze gene expression in CD4(+) T cells from the pancreatic draining lymph nodes of NOD/BDC 2.5 T cell receptor transgenic and WT NOD mice at different ages. At 4 and 6 weeks of age, we found up-regulation of a number of genes that are known to be induced by IFN-alpha. IFN-alpha levels and IFN-alpha-producing plasmacytoid dendritic cells were increased in the PLNs of 3- to 4-week-old NOD mice. Moreover, blockade of IFN-alpha receptor 1 in NOD mice by a neutralizing antibody at 2-3 weeks of age significantly delayed the onset and decreased the incidence of type 1 diabetes, increased the relative number of immature dendritic cells in the PLNs, and enhanced the ability of spleen CD4(+) T cells to produce IL-4 and IL-10. These findings demonstrate that IFN-alpha in the PLNs is an essential initiator in the pathogenesis of type 1 diabetes in NOD mice.

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Islet-Autonomous Inflammatory Signaling Propagates Autoimmunity and Promotes Diabetes in Nonobese Diabetic Mice

Project description:Type 1 diabetes (T1D) is an immune-mediated disease that leads to β cell dysfunction and death. However, the contribution of β cells in this process remains unclear. To understand how islet-derived pro-inflammatory signaling pathways contribute to diabetes pathogenesis, we generated inducible islet-specific Alox15 knockout mice on the NOD background. We report that islet-specific deletion of Alox15 induced a substantial increase of β-cell mass and decreased islet insulitis, and ultimately lead to a protection against spontaneous autoimmune diabetes in NOD mice. Single cell RNA-sequencing and mass spectrometry analysis revealed that islet-specific knockout of Alox15 leads to an increase of β cells expressing Pd-l1 and promotes an anti-inflammatory phenotype in myeloid cells and T cells inside the islets. Furthermore, islet- specific Alox15 deletion enhances the expansion of M2-like macrophages and regulatory T cells in the pancreatic islets and pancreatic lymph nodes. Together, these results lead to the conclusion that proinflammatory signals produced by β cells allows these cells to express immunoregulators that protects these cells of immune cell attack and promote β cell survival.

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IFN-alpha induced gene expression profile in NOD/BDC2.5 and NOD mice.

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2020-11-12 | GSE159547 | GEO

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 between islets from NOD-Rag and NOD-Idd22 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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