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Crinophagic granules in pancreatic β cells contribute to mouse autoimmune diabetes by diversifying pathogenic epitope repertoire

ABSTRACT: Crinophagic granules in pancreatic β cells contribute to mouse autoimmune diabetes by diversifying pathogenic epitope repertoire

PROVIDER: PRJNA1149809 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30299100_1.fastq.gz	Fastqsanger.gz
	SRR30299100_2.fastq.gz	Fastqsanger.gz
	SRR30299101_1.fastq.gz	Fastqsanger.gz
	SRR30299101_2.fastq.gz	Fastqsanger.gz
	SRR30299102_1.fastq.gz	Fastqsanger.gz

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Crinophagic granules in pancreatic β cells contribute to mouse autoimmune diabetes by diversifying pathogenic epitope repertoire

Project description:We examined the transcriotional changes in antigen specific CD4 T cells to antigens derived from thymus or to the antigens derived from islets in the autoimmune diabetes mouse model.

2024-09-06 | GSE275211 | GEO

Regulatory T cells targeting a pathogenic MHC class II: Insulin peptide epitope postpone spontaneous autoimmune diabetes

Project description:In spontaneous type 1 diabetes (T1D) non-obese diabetic (NOD) mice, the insulin B chain peptide 9-23 (B:9-23) can bind to the MHC class II molecule (IAg7) in register 3 (R3), creating a bimolecular IAg7/InsulinB:9-23 register 3 conformational epitope (InsB:R3). Previously, we showed that the InsB:R3-specific chimeric antigen receptor (CAR), constructed using an InsB:R3-monoclonal antibody, could guide CAR-expressing CD8 T cells to migrate to the islets and pancreatic lymph nodes. Regulatory T cells (Tregs) specific for an islet antigen can broadly suppress various pathogenic immune cells in the islets and effectively halt the progression of islet destruction. Therefore, we hypothesized that InsB:R3 specific Tregs would suppress autoimmune reactivity in islets and efficiently protect against T1D. To test our hypothesis, we produced InsB:R3-Tregs and tested their disease-protective effects in spontaneous T1D NOD CD28-/- mice. InsB:R3-CAR expressing Tregs secrete IL-10 dominated cytokines upon engagement with InsB:R3 antigens. A single infusion of InsB:R3 Tregs delayed the onset of T1D in 95% of treated mice, with 35% maintaining euglycemia for two healthy lifespans, while whereas control Tregs did not. Our data demonstrate that Tregs specific for MHC class II: Insulin peptide epitope (MHCII/Insulin) protect mice against T1D more efficiently than polyclonal Tregs lacking islet antigen specificity, suggesting that the MHC II/insulin-specific Treg approach is a promising immune therapy for safely preventing T1D.

2023-07-24 | GSE238146 | GEO

Regulatory T cells targeting a pathogenic MHC class II: Insulin peptide epitope postpone spontaneous autoimmune diabetes

Project description:Regulatory T cells targeting a pathogenic MHC class II: Insulin peptide epitope postpone spontaneous autoimmune diabetes

| PRJNA998046 | ENA

Autoimmune peptide antigen reactivity in BXD2 mice with spontaneous systemic autoimmune disease

2015-02-28 | GSE65276 | GEO

Autoimmune peptide antigen reactivity in BXD2 mice with spontaneous systemic autoimmune disease

Project description:The aim of the study was to determine autoimmune BXD2 mouse sera reactivity to linear peptide epitopes from the Immune Epitope Database. Pooled sera from six 8-10 month old BXD2 mice was diluted at 1:1000 and incubated on a PEPperPRINT peptide microarray platform printed with peptide autoantigens. In this study, pooled sera from six 8-10 month old BXD2 mice was profiled for anti-mouse IgG (H+L) analysis of autoantibody reactivity to peptide auto-epitopes printed in duplicate on a PepperPrint Chip.

2015-02-28 | E-GEOD-65276 | biostudies-arrayexpress

AD Granules

Project description:Study of Anaerobic Digester granules communities.

| PRJEB40014 | ENA

Antigen presentation by B cells enables epitope spreading across an MHC barrier

Project description:A progressive increase in the breadth and specificity of autoantibodies over time, termed epitope spreading, drives pathogenic targeting of an ever-widening repertoire of self-components in many autoimmune diseases. Ostensibly, this progressive inclusion of additional B cell clones into an ongoing autoreactive response can occur through linked recognition, whereby proto-autoreactive B cells recognize distinct antigenic epitopes, which carry shared T cell epitopes. In a murine model displaying epitope spreading resembling that observed in systemic lupus erythematosus, we find that the epitope spreading process is compartmentalized by MHC. Antigen presentation by B cells carrying two MHC haplotypes can bridge the MHC barrier between two compartments of B cells that do not share MHC haplotypes, by communicating with two separate pools of MHC-restricted T cells. This leads to inclusion of distinct and diverse B cell reactivities in germinal centers. Our findings demonstrate a formidable capacity of B cells to drive the autoreactive response.

2022-07-01 | GSE202358 | GEO

RNA damage compartmentalization by DHX9 granules

Project description:Cell division ensures that both genetic information and non-genetic contents are inherited by daughter cells. Whereas considerable detail has been learned about the processing of intact or damaged DNA during the cell cycle (Branzei & Foiani, 2008; Klaasen et al., 2022),(Bakhoum & Cantley, 2018),(Hustedt & Durocher, 2016), how daughter cells deal with other forms of inherited damage is unknown. Here we identified a special kind of cytoplasmic granules responsible for the compartmentalisation of parental RNA damage. We found that ultraviolet (UV)-induced RNA, but not DNA, damage triggered assembly of this unique type of granules characterized by the presence of RNA helicase DHX9. By developing a novel methodology, FANCI, we discovered that DHX9 granules are enriched in damaged intron RNA and pre-mRNA-binding proteins, which is in contrast to other classical stress granules (SGs) that are composed of mature mRNA. Intron damage impeded proper splicing and intron decay, and induced generation of circRNA and dsRNA in the granules. Moreover, we showed that intron damage induced DHX9 granules assembled specifically in postmitotic daughter cells and triggered a cellular dsRNA immune response. Condensation with dsRNA is crucial for DHX9 localization to the granules and the modulation of dsRNA in these granules by DHX9 was crucial for daughter cell survival. Our observations revealed that DHX9 granules constitute a dedicated non-membrane-bound cytoplasmic compartment that protects daughter cells from parental damaged RNA.

2023-11-11 | GSE218180 | GEO

Combinatorial tagging generates a multi-purpose knock-in mouse model revealing phase separation-dependent germ granules in RNA homeostasis and germline development

Project description:A large resource of epitope-tagged or Cre/CreERT2-expressing mouse models are available for study of germ granules or germline development. The germ granules are proteinaceous, membraneless organelles implicated in germ cell differentiation and maturation; however, their protein and RNA transcript constituents, and their mechanistic insight remain not fully understood. Herein, we generated a versatile germline mouse model through combinatorial tagging of DDX4 for simultaneous expression of three cistronic coding products (C-terminal tagged DDX4 - DDX45HA, EGFP, and CreERT2) under the driving control of endogenous Ddx4 promoter. By leveraging the high-affinity HA tag, we optimized an efficient workflow for purification of germ granules (Chromatoid body, CB) from spermatids, and characterized the landscape of protein constituents and RNA transcripts in CB. Moreover, we explored and ascertained that DDX4-mediated, phase-separation dependent CB integrity is functionally important for recruiting distinctive long RNA transcripts and biogenesis of pachytene- and TE-derived piRNAs. Together, our study generated a versatile germline mouse model with a multiplicity of applications for germline study, and provided mechanistic insight into germline development as dictated by germ granules.

2024-08-05 | GSE273344 | GEO

CSR-1 and P granules suppress sperm-specific transcription in the C. elegans germline

Project description:P granules in C. elegans are required for fertility and function to maintain germ cell identity and pluripotency. Sterility in the absence of P granules is often accompanied by the mis-expression of soma-specific proteins and the initiation of somatic differentiation in germ cells. To investigate whether this is caused by the accumulation of somatic transcripts, we performed mRNA-seq on dissected germlines with and without P granules. Strikingly, we found that somatic transcripts do not increase in the young adult germline when P granules are impaired. Instead, we found that impairing P granules causes sperm-specific mRNAs to become highly overexpressed. This includes the accumulation of major sperm protein (MSP) transcripts in germ cells, a phenotype that is suppressed by feminization of the germline. A core component of P granules, the endo-siRNA-binding Argonaute protein CSR-1, has recently been ascribed with the ability to license transcripts for germline expression. However, impairing CSR-1 has very little effect on the accumulation of its mRNA targets. Instead, we found that CSR-1 functions with P granules to prevent MSP and sperm-specific mRNAs from being transcribed in the hermaphrodite germline. These findings suggest that P granules protect germline integrity through two different mechanisms, by 1) preventing the inappropriate expression of somatic proteins at the level of translational regulation, and by 2) functioning with CSR-1 to limit the domain of sperm-specific expression at the level of transcription. Four biological replicates of each condition (empty vector control, P granule RNAi, and CSR-1 RNAi germlines) were collected for total RNA.

2015-05-20 | E-GEOD-67954 | biostudies-arrayexpress

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