Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA251856 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report the single-cell RNA sequencing data obtained from BCL1 lymphoma-bearing mice treated with either isotype control, anti-CD20 mAb, anti-CD27 mAb or anti-CD20+anti-CD27 mAb together
2018-01-12 | GSE97037 | GEO
Project description:The clinical utility of T-cell agonistic antibodies in cancer therapy, much less their ability to stimulate intratumoral T-cells in patients, has eluded us. T-cell agonistic antibodies such as anti-CD27 can induce clinically meaningful anti-tumor activity. The combination of anti-CD27 agonist varlilumab and tumor-depleting anti-CD20 rituximab was investigated in patients with relapsed/refractory B-cell non-Hodgkin lymphoma (B-NHL) (RiVa trial;NCT03307746). Our experiments detail scRNA-seq data from 6 B-cell NHL patients, including both pre and on-treatment biopsies taken from lymph nodes.
2025-08-09 | E-MTAB-14585 | biostudies-arrayexpress
Project description:The clinical utility of T-cell agonistic antibodies in cancer therapy, much less their ability to stimulate intratumoral T-cells in patients, has eluded us. T-cell agonistic antibodies such as anti-CD27 can induce clinically meaningful anti-tumor activity. The combination of anti-CD27 agonist varlilumab and tumor-depleting anti-CD20 rituximab was investigated in patients with relapsed/refractory B-cell non-Hodgkin lymphoma (B-NHL) (RiVa trial;NCT03307746). Our experiments detail RNA-seq data from 21 B-cell NHL patients, including both pre and on-treatment biopsies taken from lymph nodes.
2025-08-09 | E-MTAB-14594 | biostudies-arrayexpress
Project description:CD137 is a costimulatory receptor expressed on natural killer cells, T cells, and subsets of dendritic cells. An agonistic monoclonal antibody (mAb) against CD137 has been used to reduce tumor burden or reverse autoimmunity in animal models and clinical trials. When testing the ability of agonistic anti-CD137 mAb to promote clearance of persistent virus infection, we recently reported reduced numbers of germinal center B (GC B) cells and follicular dendritic cells (FDC) in lymphoid tissues. Here, we show that agonistic anti-CD137 agonistic mAb treatment impairs antibody responses with multiple T cell-dependent antigens including virus infection, recombinant viral antigens, and conjugated haptens but not with a T cell-independent antigen or at homeostasis. These effects were not due to enhanced apoptosis or impaired proliferation of B cells but instead correlated with disorganization of the stromal cell compartment of the GC, and were mediated by CD137 signaling in CD4+ and CD8+ T cells. Anti-CD137 treatment in the context of acute infection also resulted in reduced numbers of marginal zone B cells, greater numbers of antibody-secreting plasmablasts, and pro-inflammatory signatures in several myeloid and lymphoid cell populations of the spleen. Our experiments in mice suggest that agonistic anti-CD137 mAbs used in cancer and autoimmunity therapy may alter stromal cell populations to causes GC collapse and impaired long-term antibody and B cell memory responses.
2019-12-31 | GSE141117 | GEO
Project description:CD137 is a costimulatory receptor expressed on natural killer cells, T cells, and subsets of dendritic cells. An agonistic monoclonal antibody (mAb) against CD137 has been used to reduce tumor burden or reverse autoimmunity in animal models and clinical trials. When testing the ability of agonistic anti-CD137 mAb to promote clearance of persistent virus infection, we recently reported reduced numbers of germinal center B (GC B) cells and follicular dendritic cells (FDC) in lymphoid tissues. Here, we show that agonistic anti-CD137 agonistic mAb treatment impairs antibody responses with multiple T cell-dependent antigens including virus infection, recombinant viral antigens, and conjugated haptens but not with a T cell-independent antigen or at homeostasis. These effects were not due to enhanced apoptosis or impaired proliferation of B cells but instead correlated with disorganization of the stromal cell compartment of the GC, and were mediated by CD137 signaling in CD4+ and CD8+ T cells. Anti-CD137 treatment in the context of acute infection also resulted in reduced numbers of marginal zone B cells, greater numbers of antibody-secreting plasmablasts, and pro-inflammatory signatures in several myeloid and lymphoid cell populations of the spleen. Our experiments in mice suggest that agonistic anti-CD137 mAbs used in cancer and autoimmunity therapy may alter stromal cell populations to causes GC collapse and impaired long-term antibody and B cell memory responses.
2019-12-31 | GSE141111 | GEO
Project description:CD27, a member of the tumor necrosis factor receptor super family (TNFRSF7), is constitutively expressed on the majority of mature T cells, memory B cells, and a portion of NK cells. Here we report on the 1F5-induced immune modulation of isolated human T cells. In vitro activation of peripheral blood-derived T cells from different healthy volunteers with mAb 1F5 showed that crosslinking of CD27 in the presence of CD3 stimulation (OKT3 mAb) was essential to elicit proliferation and broad spectrum of cytokine release. Analysis of this response on a multiplex cytokine array system revealed a Th1-biased cytokine profile (IFN-gamma, IL-2 and TNF-alpha). Transcriptional profiling by microarray RNA hybridization is underway to map specific and global gene expression changes following 1F5 modulation of T cells.
2015-07-17 | GSE58267 | GEO
Project description:B cell receptor (BCR) is essential in activating B cells and mediating the immune responses. Analyzing the BCR-triggered gene expression would help delineate the regulatory function of B cells. The mouse B cells were treated with anti-IgM mAb to mimic the BCR stimulation, and the genome-wide transcriptional responses were analyzed by using high-throughput sequencing at high-temporal resolution (24 time points over 6 hours).
2019-04-10 | GSE129536 | GEO
Project description:Transcriptomic data of B-cell lymphoma bearing mice treated with anti-CD20/-CD27 mAb therapy
| PRJNA380509 | ENA
Project description:Dorsomorphin is a small molecule inhibitor of type I bone morphogenic protein receptors (BMPRs). We have found that dorsomorphin affects a wide range of T cell function. In order to obtain the bigger picture of the effects of DM in T cell activation. transcriptomic analysis was performed using mouse primary CD25-CD4+ T cells with either DM (4 μM) or vehicle in the presence or absence of stimulation by anti-CD3 and -CD28 antibodies. Mouse CD4+ T cells were prepared and cultured with or without stimulation by plate bound anti-CD3 mAb and soluble anti-CD28 mAb for 1 hour. Subsequently, 4 μM DM or DMSO was added and cells were incubated for 6 hours. Total RNA was isolated using Qiagen RNeasy mini kits.
2011-12-01 | E-GEOD-27378 | biostudies-arrayexpress
Project description:To study the effect of CD27 triggering on HSC biology Ageing of the hematopoietic stem cell (HSC) compartment is characterized by an accumulation of less productive HSCs with impaired lymphoid differentiation capacity, which contributes to age-dependent hematological abnormalities including anemia, myeloproliferative disorders and a decline in adaptive immunity. Since HSCs express the costimulatory receptor CD27 and because inflammation has been associated with HSC ageing, we investigated the effect of stimulation of CD27 by its inflammatory ligand CD70 on HSC maintenance. We found that CD27-triggering during CD70-driven immune activation in young mice enhances HSC self-renewal, leading to accumulation of HSCs to levels comparable with old control mice. These findings indicate that CD27-signaling accelerates HSC ageing, which is supported by the observation that CD27-triggering negatively affects HSC differentiation to the lymphoid lineage and increases myeloid differentiation. This functional change was mirrored by a corresponding difference in gene expression, as microarray analysis indicated that CD27-triggered HSCs have a strongly myeloid-biased gene signature. CD27 signaling also induced enrichment of genes associated with biological processes involved in cellular responses to DNA damage/repair and reactive oxygen species (ROS), which are associated with HSC ageing and related to increased proliferation. Therefore, we postulate that CD27 triggering during chronic inflammation contributes directly to ageing of the hematopoietic compartment.
2014-12-31 | GSE31574 | GEO