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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [BCR-Seq]

ABSTRACT: Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [BCR-Seq]

PROVIDER: PRJNA784304 | ENA |

REPOSITORIES: ENA

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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma

Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma

| PRJNA784301 | ENA

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [BCR-Seq]

Project description:Two percent of children with Neuroblastoma, a pediatric solid tumor of the peripheral nerve ganglia, develop Opsoclonus Myoclonus Ataxia Syndrome (OMAS), a paraneoplastic disease characterized by devastating cerebellar and brainstem-directed autoimmunity, but typically with outstanding cancer-related outcomes. Here, we compared tumor transcriptomes and tumor infiltrating T- and B-cell repertoires from a cohort of OMAS subjects with neuroblastoma to a set of controls from 13 low- and 13 high-risk non-OMAS associated neuroblastoma tumors.

2023-08-01 | GSE189741 | GEO

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [TCR-Seq]

Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [TCR-Seq]

| PRJNA784303 | ENA

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [RNA-Seq]

Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [RNA-Seq]

| PRJNA782665 | ENA

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [TCR-Seq]

2023-08-01 | GSE189742 | GEO

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [RNA-Seq]

2023-08-01 | GSE189367 | GEO

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma

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

2023-08-01 | GSE189743 | GEO

Mercury intoxication disrupts tonic signaling in B cells, and may promote autoimmunity due to abnormal phosphorylation of STIM-1 and other autoimmunity risk associated phosphoproteins involved in BCR signaling

Project description:Epidemiological studies link exposure to mercury with autoimmune disease. Unfortunately, in spite of considerable effort, no generally accepted mechanistic understanding of how mercury actually functions with respect to the etiology of autoimmune disease is currently available. Nevertheless, autoimmune disease often arises because of defective B cell signaling. Because B cell signaling is dependent on phosphorylation cascades, in this report, we have focused on how mercury intoxication alters phosphorylation of B cell proteins in antigen-non stimulated (tonic) mouse splenic B cells. Specifically, we utilized mass spectrometric techniques to conduct a comprehensive unbiased global analysis of the effect of mercury on the entire B cell phosphoproteome. We found that the effects were pleotropic in the sense that large numbers of pathways were impacted. However, confirming our earlier work, we found that the B cell signaling pathway stood out from the rest, in that phosphoproteins which had sites which were affected by mercury, exhibited a much higher degree of connectivity, than components of other pathways. Further analysis showed that many of these BCR pathway proteins had been previously linked to autoimmune disease. Finally, dose response analysis of these BCR pathway proteins showed STIM1_S575, and NFAT2_S259 are the two most mercury sensitive of these sites. Because STIM1_S575 controls the ability of STIM1 to regulate internal Ca2+, we speculate that STIM1 may be the initial point of disruption, where mercury interferes with B cell signaling leading to systemic autoimmunity, with the molecular effects pleiotropically propagated throughout the cell by virtue of Ca2+ dysregulation.

2024-10-17 | PXD042189 | Pride

Mechanistic characterization of a Drosophila model of paraneoplastic nephrotic syndrome

Project description:Purpose: Paraneoplastic syndromes occur in cancer patients and originate from dysfunction of organs at a distance from the tumor or its metastasis. In this study, using a Drosophila gut tumor model, we characterized a mechanism of tumor-induced kidney dysfunction. Methods: snRNA-seq analysis of MT samples with and without Yki gut tumors and snRNA-seq analysis of MT samples with kidney principal cell-specific disregulation of PDGF/VEGF signaling Results: we found that Pvf1, a PDGF/VEGF signaling ligand, secreted by gut tumors activates the PvR/JNK/Jra signaling pathway in the principal cells of the kidney, leading to mis-expression of renal genes and paraneoplastic renal syndrome-like phenotypes Conclusions: Our study describes a novel mechanism by which gut tumors perturb the function of the kidney, which might be of clinical relevance for the treatment of paraneoplastic syndromes.

2024-01-18 | GSE251715 | GEO

Circadian Clock Protein CRY Regulates Autoimmunity

Project description:The circadian system regulates numerous physiological processes including the adaptive immune system. Here we show that mice deficient for the circadian genes Cry1 and Cry2, (DKO) display an autoimmune phenotype including higher serum IgG concentration, presence of serum anti-nuclear antibodies, precipitation of IgG, IgM and complement 3 in glomeruli, and massive infiltrations of leukocytes into the lung and kidney. Activation of Cry DKO splenic B cells elicited markedly enhanced and prolonged tyrosine phosphorylation of cellular proteins compared to cells from control mice, suggesting that over activation of the BCR signaling pathway may contribute to autoimmunity in the Cry DKO mice. Expression of C1q, deficiency of which contributes to the pathogenesis of Systemic lupus erythematosus (SLE), was significantly downregulated in Cry DKO B cells. This suggests that B cell development, BCR signaling pathway and C1q expression may be under direct circadian control and dysregulation of which contributes to autoimmunity.

2018-08-24 | GSE87467 | GEO

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