Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA254536 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:CD30 receptor (TNFRSF8) is highly expressed in some types of lymphoma. CD30 is successfully used as a target for antibody-drug conjugate to treat CD30+ lymphoma. The agonistic activity of the anti-CD30 antibody likely contributes to tumor cell killing. However, not all antibodies exhibit agonistic activity. We found that potent agonistic antibodies recognize the N-terminus epitope cluster that is distantly located from the ligand binding site of CD30. This study compared gene expression profiles between CD30 natural ligand and agonistic antibody T104 treatment in a CD30+ ALCL Karpas 299 cell line.
2025-08-10 | GSE59174 | GEO
Project description:CD30 receptor (TNFRSF8) is highly expressed in some types of lymphoma. Therefore, CD30 is successfully used as a target for antibody-drug conjugate to treat CD30+ lymphoma. In this study, we compared gene expression profiles induced in CD30+ L540 cell line by treating CD30 natural ligand or anti-CD30 antibodies against different epitopes.
2025-08-10 | GSE67794 | GEO
Project description:CD30L and CD30 are cell-surface glycoproteins in the TNF and TNFR superfamilies, respectively. Their expression is limited to immune cells and is tightly regulated. Cell surface expression of CD30 is restricted to subpopulations of activated T and B cells. CD30L is expressed primarily on activated T cells and subpopulations of B cells. The significance of CD30/CD30L interactions in immune regulation is not fully understood. Reported activities of CD30/CD30L in immune responses imply roles in regulation of secondary memory and antibody responses. Depending on the experimental system, both positive and negative regulation of immunoglobulin class switching and antibody production have been reported. Additionally, the biological activity of CD30/CD30L in animals has been difficult to assess due to the restricted and tightly regulated expression of this receptor-ligand pair. We generated transgenic mice with constitutive T cell specific overexpression of CD30L as a tool to help unravel the consequences of CD30/CD30L interactions in vivo. CD30L transgenic mice displayed a phenotype and responses to antigen challenge supporting a role for CD30/CD30L in promoting immunoglobulin class switching and antibody production. CD30L transgenic mice had increased numbers of germinal centers, elevated class-switched immunoglobulin isotypes, increased germinal center B cells and plasma cells, upregulation of genes indicative of B-cell activity, and exaggerated antibody responses to immune challenge. Interestingly, despite the heightened B-cell activity in CD30L transgenic mice, CD30L overexpression on T cells did not result in overt autoimmunity. Our results demonstrate that overexpression of CD30L on T cells promotes T cell-dependent B cell responses characterized by secondary antibody responses. Experiment Overall Design: Spleen, thymus, mesenteric lymph nodes and peripheral lymph nodes where samples from both CD30L transgenic and non-transgenic littermates (4 mice per group.)
2008-06-16 | E-GEOD-8039 | 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:CD30L and CD30 are cell-surface glycoproteins in the TNF and TNFR superfamilies, respectively. Their expression is limited to immune cells and is tightly regulated. Cell surface expression of CD30 is restricted to subpopulations of activated T and B cells. CD30L is expressed primarily on activated T cells and subpopulations of B cells. The significance of CD30/CD30L interactions in immune regulation is not fully understood. Reported activities of CD30/CD30L in immune responses imply roles in regulation of secondary memory and antibody responses. Depending on the experimental system, both positive and negative regulation of immunoglobulin class switching and antibody production have been reported. Additionally, the biological activity of CD30/CD30L in animals has been difficult to assess due to the restricted and tightly regulated expression of this receptor-ligand pair. We generated transgenic mice with constitutive T cell specific overexpression of CD30L as a tool to help unravel the consequences of CD30/CD30L interactions in vivo. CD30L transgenic mice displayed a phenotype and responses to antigen challenge supporting a role for CD30/CD30L in promoting immunoglobulin class switching and antibody production. CD30L transgenic mice had increased numbers of germinal centers, elevated class-switched immunoglobulin isotypes, increased germinal center B cells and plasma cells, upregulation of genes indicative of B-cell activity, and exaggerated antibody responses to immune challenge. Interestingly, despite the heightened B-cell activity in CD30L transgenic mice, CD30L overexpression on T cells did not result in overt autoimmunity. Our results demonstrate that overexpression of CD30L on T cells promotes T cell-dependent B cell responses characterized by secondary antibody responses. Keywords: Transgenic vs. wild-type
2007-10-30 | GSE8039 | GEO
Project description:A proteomic analysis using co-immunoprecipitations (Co-IPs) coupled to mass spectrometry to compare the FLS2 interactomes induced by the natural ligand or the surrogates.
proFLS2:FLS2-GFP line was used for treatment either DMSO, Maya1, Maya2, or flg22 and wild-type (Col 0) was used for negative control treatment with flg22.
2024-09-27 | PXD056313 | JPOST Repository
Project description:Chicken MarekM-bM-^@M-^Ys disease (MD) is a unique naturally occurring model for human herpesvirus-induced lymphomas that over-express the M-bM-^@M-^\HodgkinM-bM-^@M-^Ys disease antigenM-bM-^@M-^] (TNFRSF-8; CD30) on the lymphomaM-bM-^@M-^Ys neoplastically-transformed cells. We used transcriptomics, proteomics, computational systems biology and reductionist molecular biology to identify the differences between the CD30(hi) lymphoma cells and the non-transformed CD30(lo) MD lymphoma cells. We propose specific mechanisms of neoplastic transformation, genetic resistance to lymphomagenesis and impact of lymphoma microenvironment on CD30(hi) cell development. We demonstrate that: a) in situ, CD30(lo) cells are pre-neoplastic and we identify the proteome involved in transformation as well as potential mechanisms that may be controlled by MDV oncogene Meq; b) MD herpesvirus, (via its Meq oncogene) can drive a feed forward loop that induces CD30 transcription and overexpression, increased CD30 signaling, which then activates NFM-NM-:B and, in turn, increases Meq transcription; c) Meq transcriptional repression or activation from the CD30 promoter generally correlates with a polymorphism in the CD30 promoter between MD-resistant and -susceptible chicken genotypes and so a herpesvirus has evolved to utilize NFM-NM-:B as a direct transcriptional activator for its oncogene. A dual color, balanced design was carried on eight sorted lymphoma cells from white leghorn chickens infected with MDV GA/22 strain. Each of two sample types, CD30(hi) and CD30(lo) cells, includes four biological replicates for total RNA extraction and labeling. A Dye swap was used in four biological repeats of CD30(hi) to CD30(lo) cells comparison. Background subtracted signal intensities were collected from 4 arrays and normalized for data analysis.
2012-03-15 | E-GEOD-28034 | biostudies-arrayexpress
Project description:CD200R is an immune checkpoint receptor of the IgG family that is primarily expressed on cells of the myeloid lineage. In vivo studies with knockout mice of either the receptor or its ligand, CD200, have demonstrated that it is an inhibitory receptor capable of negatively regulating immune responses. Previous work using agonistic antibodies to mouse CD200R showed inhibition of mast cell activation in multiple preclinical models of autoimmune diseases. We developed an agonistic antibody to the human CD200 receptor to downregulate the immune system human inflammatory conditions. Ucenprubart, is a humanized IgG4 monoclonal antibody that binds and agonizes human CD200R to suppress cellular activity in CD200R-expressing cells.The antibody was engineered to have desired properties for agonism and cross-reactivity to cyno CD200R. In vivo the antibody demonstrated efficacy in a humanized mouse model of contact hypersensitivity as well as passive cutaneous anaphylaxis in cynomolgus monkeys.
2025-02-08 | GSE220685 | GEO
Project description:Small subsets of B cells in the germinal center (GC) and in extrafollicular regions of lymph nodes express the activation marker CD30. Very little is known about the specific features of these cells and their relationship to the CD30-expressing Hodgkin and Reed/Sternberg (HRS) cells of Hodgkin lymphoma. Phenotypic and immunoglobulin V gene analyses revealed that CD30+ GC B lymphocytes represent typical GC B cells, and that CD30+ non-GC B cells are mostly post-GC B cells. However, despite these seemingly distinct identities, both CD30+ subsets share an unexpectedly large overlap in specific transcriptome patterns, and are strikingly different from bulk GC B cells and classical memory and plasma cells, respectively. A main common feature of these CD30+ B cells is a strong MYC signature. CD30+ GC B cells appear to represent the recently described MYC+ GC B cell subset of recirculating centrocytes at the stage of centroblast transition. CD30+ non-GC B cells rather represent highly activated and proliferating memory B cells, differentiating into plasma cells. Notably, CD30+ B cells were more similar in their transcriptome patterns to HRS cells than any other B cell subset investigated, suggesting that HRS cells may either derive from CD30+ B cells or acquired a similar activation signature. In comparison to CD30+ B cells and other lymphomas, HRS cells show a remarkable downregulation of genes regulating cell cycle, genomic stability and polyploidity, providing a potential explanation for the genomic instability and multinuclearity of HRS cells.
2018-06-13 | GSE83441 | GEO