Ontology highlight
ABSTRACT:
PROVIDER: PRJNA876642 | ENA |
REPOSITORIES: ENA
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Project description:The tumoricidal effects of CD8+T cells are well acknowledged, but how MHC Ib-restricted CD8+T (Ib-CD8+T) cells contribute to anti-tumor immunity remains obscure. Here, we show that infusion of MHC Ia+ cells to Kb-/-Db-/- mice induced the expansion of Ib-CD8+T cells in tumors and potently inhibited tumor progression. Such priming of Ib-CD8+T cells by MHC-Ia is not MHC haplotype restricted and MHC Ia tetramers alone can prime Ib-CD8+T cells for activation. The MHC Ia priming promoted Tbet expression in Ib-CD8+T cells and in absence of Tbet, such priming effect diminished. Importantly, these tumoricidal Ib-CD8+T cells are positive for CX3CR1, and exhibit rapid proliferation, high expression of cytotoxic factors, and prolonged persistence at tumor sites. Adoptive transfer of CX3CR1+Ib-CD8+T cells to wild type mice resulted in potent anti-tumor effects. Our findings unravel an uncharacterized function of MHC Ia molecules in immunoregulation and raise the possibility of using Ib-CD8+T cells in tumor immunotherapy.
2023-10-03 | GSE164271 | GEO
Project description:Background: Glycogen Storage Disease (GSD) Type Ia and Ib are rare metabolic diseases caused by gene variants in G6PC and SLC37A4 respectively. Patients often suffer from multiple metabolic abnormalities and severe long-term complications. Methods: In this study, we employed comprehensive untargeted proteomics on retrospectively registered samples: 26 serum/plasma samples (18 GSD Ia and 8 GSD Ib) from patients with 21 matched healthy controls, complemented by 4 liver samples from 3 patients who received liver transplantation (3 from GSD Ia including 1 with hepatocellular carcinoma tissue and 1 from GSD Ib), compared to 10 donor liver samples, to investigate the pathological mechanisms of disease complications and identify potential biomarkers. Results: Pathway analysis of the differentially regulated proteins revealed distinct changes in the serum/plasma of GSD Ia and Ib. Coagulation was the most significantly changed biological process in the GSD Ia patients. Immune response-associated proteins, especially a large number of immunoglobulins, increased in GSD Ib specifically. Proteins related to liver injury, cholesterol, and amyloidosis were altered in two subtypes, though more pronounced in GSD Ia. Potential biomarkers with significant alterations both in the circulation as well as in the liver were identified specifically for monitoring and prognosing GSD Ia (COL163 and PROC), GSD Ib (F11 and CD163), and hepatocellular carcinoma (HCC) in GSD Ia patients (ALDOB and CFHR5). Conclusions: These findings provide new insights into the pathogenesis of GSD I-related complications and highlighted the potential of protein circulating biomarkers for monitoring complication progression in GSD Ia and Ib, as well as for assessing HCC risk in GSD Ia patients.
2026-03-06 | PXD066805 | Pride
Project description:Glycogen storage disease type I (GSD I) is an autosomal recessive inborn error of carbohydrate metabolism. Patients with GSD type Ia and Ib exhibit overlapping and distinct symptoms and complications. Notably, GSD Ia patients show more severe hypertriglyceridemia and higher risk of hepatic tumors than GSD Ib patients. Given the liver's pivotal role in these processes, this study utilized hepatocyte-specific CRISPR/Cas9-mediated gene editing to explore the pathophysiological and biochemical differences between hepatic GSD Ia and Ib. Additionally, hepatic histology, transcriptomics, and proteomics analysis was performed. Compared to controls, GSD Ia and Ib mice showed hepatomegaly, fasting hypoglycemia, hyperlactatemia, and increased uric acid in plasma, which was more pronounced in GSD Ia than Ib. Both GSD I subtypes showed similar reductions in hepatic acetyl-CoA precursor pool enrichment and inceases in de novo biosynthesis of hepatic stearate and oleate. Interestingly, only GSD Ia mice showed significantly elevated plasma triglyceride, uric acid, and hepatic phosphate sugars. These metabolic changes were reflected at the level of transcriptomics and proteomics results. Moreover, altered mRNAs and protein levels related to nucleotide-binding oligomerization domain (NOD) signaling pathways, infection and inflammation, liver disease, and chemical carcinogenesis were more pronounced in GSD Ia mice. Overall, the metabolic disturbance was more severe in hepatocyte-specific GSD Ia than Ib mice, consistent with the clinical phenotype on patients. The metabolic disorders and specific metabolites, genes, and proteins identified in this study provided new insights into the potential therapeutic targets for GSD I patients, highlighting the need for subtype-specific treatment strategies.
2026-07-02 | PXD066807 | Pride
Project description:This data presents the complete proteomic subcellular characterization (extracellular secreted proteins, cell wall-associated proteins, cytosolic proteins, crude membrane proteins, peripheral membrane proteins and proteins present in purified membranes) of Streptococcus pyogenes serotype M1 (strain AP1).
2017-04-20 | MSV000080971 | MassIVE
Project description:The human-derived serotype Ⅴ ST1 GBS strains NNA038 and NNA048 was isolated from a amniotic fluid of full-term pregnant woman who suffered from premature rupture of membrane in China.Serotype Ia ST7 GBS strain YM001 is an attenuated strain ,its parent strain HN016 was isolated from an outbreak epidemical disease in tilapia from China.HN016_KO_D2 is a knockout strain from Serotype Ia ST7 GBS strain HN016.
2019-11-12 | PXD011206 | Pride