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Targeting BMI-1 to deplete antibody-secreting cells in autoimmunity

ABSTRACT: We measured genes expression differences in antibody secreting cells from LynKO mice in following treatment with a BMI-1 inhibitor (PTC-028) or a vehicle control. BMI-1 inhibition lead to a reduction in antibody secreting cells in LynKO mice and in humans donors. We performed RNA sequencing to understand the impact of BMI-1 inhibition on antibody secreting cells in LynKO mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE239515 | GEO | 2023/10/05

REPOSITORIES: GEO

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Targeting BMI-1 to deplete antibody-secreting cells in autoimmunity

Project description:Targeting BMI-1 to deplete antibody-secreting cells in autoimmunity

| PRJNA999632 | ENA

Targeting BMI-1 to deplete antibody-secreting cells in autoimmunity.

Project description:ObjectivesB cells drive the production of autoreactive antibody-secreting cells (ASCs) in autoimmune diseases such as Systemic Lupus Erythematosus (SLE) and Sjögren's syndrome, causing long-term organ damage. Current treatments for antibody-mediated autoimmune diseases target B cells or broadly suppress the immune system. However, pre-existing long-lived ASCs are often refractory to treatment, leaving a reservoir of autoreactive cells that continue to produce antibodies. Therefore, the development of novel treatment methods targeting ASCs is vital to improve patient outcomes. Our objective was to test whether targeting the epigenetic regulator BMI-1 could deplete ASCs in autoimmune conditions in vivo and in vitro.MethodsUse of a BMI-1 inhibitor in both mouse and human autoimmune settings was investigated. Lyn -/- mice, a model of SLE, were treated with the BMI-1 small molecule inhibitor PTC-028, before assessment of ASCs, serum antibody and immune complexes. To examine human ASC survival, a novel human fibroblast-based assay was established, and the impact of PTC-028 on ASCs derived from Sjögren's syndrome patients was evaluated.ResultsBMI-1 inhibition significantly decreased splenic and bone marrow ASCs in Lyn -/- mice. The decline in ASCs was linked to aberrant cell cycle gene expression and led to a significant decrease in serum IgG3, immune complexes and anti-DNA IgG. PTC-028 was also efficacious in reducing ex vivo plasma cell survival from both Sjögren's syndrome patients and age-matched healthy donors.ConclusionThese data provide evidence that inhibiting BMI-1 can deplete ASC in a variety of contexts and thus BMI-1 is a viable therapeutic target for antibody-mediated autoimmune diseases.

| S-EPMC10550498 | biostudies-literature

mRNA-seq of PTC-028 treated fusion-positive rhabdomyosarcoma cells

Project description:Purpose: This study aims to identify novel targets in the rare pediatric cancer, fusion-positive rhabdomyosarcoma (FP-RMS), and examine differences/similarities in FP-RMS tumor responses to BMI1 (B lymphoma Mo-MLV insert region 1 homolog) inhibition. Methods: FP-RMS cell lines Rh28 and Rh30 were treated with DMSO (vehicle) or PTC-028, a BMI1 inhibitor, and RNA was collected after 24 or 48 hr in triplicate. RNA-seq was performed, and gene expression data were analyzed through Gene Ontology (GO) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analyses. Data from OncoPPi and the STRING database were also utilized in this study. Results: Both Rh28 and Rh30 had some overlapping pathways affected by PTC-028, notably downregulation of cell cycle progression, the DNA damage response, and cholesterol biosynthesis. Rh30+PTC-028 had more genes containing TEAD-motifs downregulated compared to Rh28+PTC-028. Rh28 and Rh30 also had differing changes in expression in kinases of LATS1/2, EPHA2, and PDGFRA. Conclusion: Overall, these results bring new insights into pathways influenced by BMI1 expression and contrasting intertumor drug responses in FP-RMS.

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Project description:Bmi-1 and Mel-18 are close structural homologues that belong to the polycomb group (PcG) of transcriptional regulators of homeotic gene expression in development. They are believed to stably maintain repression of gene expression by altering the state of chromatin at specific promoters. A number of clinical and experimental observations have also implicated Bmi-1 in tumorigenesis and stem cell maintenance. Bmi-1 overexpression or amplification has been observed in a number of human malignancies, particularly in B-cell lymphomas, medulloblastomas and breast cancer. We report here that shRNA-mediated knock-down of either Bmi-1 or Mel-18 in human medulloblastoma DAOY cells results in the inhibition of proliferation, loss of clonogenic survival and anchorage-independent growth, and suppression of xenograft tumor formation in nude mice. Furthermore, overexpression of both Bmi-1 and Mel-18 significantly increased clonogenic survival of Rat1 fibroblasts. In contrast, stable downregulation of Bmi-1 or Mel-18 alone did not affect the growth of SK-OV-3 or U2OS cancer cell lines or normal human WI38 fibroblasts. Gene expression analysis of shRNA-expressing DAOY cells has demonstrated a significant overlap in the Bmi-1- and Mel-18-regulated genes and revealed novel gene targets under their control. Taken together, these results suggest that Bmi-1 and Mel-18 might have overlapping functions in human tumorigenesis. Keywords: shRNA knock-down

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Project description:The CD19 positive antibody secreting cells (ASC) in both bone marrow (BM) have the capacity to provide immune memory in addition to cells traditionally considered long-lived, the CD19-negative BM ASC. We performed flow cytometry (FCM) immunophenotyping, fluorescence-activated cell sorting (FACS) for cell subset isolation, ELISpot assays detecting the isotype of antibody secretion as well as antibodies against vaccine derived antigens, and comparative gene expression analyses of CD19- ASC, CD19+ ASC, CD20- B cells, and CD20+ B cells from BM. The findings may aid in the understanding of the differential cell subsets created through vaccination and lead to improved vaccine strategies and production. FACS sorted tissue B cells and antibody secreting cell subset gene expression.

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