Effect of a CD28H agonistic monoclonal antibody on NK cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA638872 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11996645.fastq.gz | Fastqsanger.gz | |||
| SRR11996646.fastq.gz | Fastqsanger.gz | |||
| SRR11996647.fastq.gz | Fastqsanger.gz | |||
| SRR11996648.fastq.gz | Fastqsanger.gz | |||
| SRR11996649.fastq.gz | Fastqsanger.gz |
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Project description:Mature NK cell activation relies on a balance of activating, co-stimulatory and inhibitory receptors involved during target recognition. Immunotherapy strategies has been developed to finely tune this balance in order to enhance NK cell cytotoxic functions against cancer cells and secretory functions to enhance adaptative immunity activation. CD28H, a new member of the CD28 family, has been recently studied in T cells and on NK cells as a part of CD28H-CAR-NKL strategy. Given the impressive expression of CD28H molecule on circulating NK cells, we evaluated the use an anti-CD28H mAb on NK cell activation.
2024-10-24 | GSE152269 | 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: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:Analysis of the effect of anti-IL-15 monoclonal antibody treatment on T cell and NK cell homeostasis in rhesus macaques. The hypothesis tested in the present study was that repeated administrations of a rhesusized anti-IL-15 monoclonal antibody would block IL-15 activity in vivo and result in changes to T and/or NK cell population dynamics that would reflect physiologic IL-15 function. The results provide important information on the specific role IL-15 plays in effector memory T cell and NK cell homeostasis, noting that effector memory T cells but not NK cells can be maintained in the absence of IL-15 signaling by the activity of other cytokines. Sort-purified CD8+ and CD4+ TCM from PBMC, before and after treatment with IgG1 Ab and anti-IL15 Ab
2016-09-07 | E-GEOD-76785 | biostudies-arrayexpress
Project description:Analysis of the effect of anti-IL-15 monoclonal antibody treatment on T cell and NK cell homeostasis in rhesus macaques. The hypothesis tested in the present study was that repeated administrations of a rhesusized anti-IL-15 monoclonal antibody would block IL-15 activity in vivo and result in changes to T and/or NK cell population dynamics that would reflect physiologic IL-15 function. The results provide important information on the specific role IL-15 plays in effector memory T cell and NK cell homeostasis, noting that effector memory T cells but not NK cells can be maintained in the absence of IL-15 signaling by the activity of other cytokines. Sort-purified CD8+ TEM from PBMC, before and after treatment with IgG1 Ab and anti-IL15 Ab
2016-09-07 | E-GEOD-76796 | biostudies-arrayexpress
Project description:Analysis of the effect of anti-IL-15 monoclonal antibody treatment on T cell and NK cell homeostasis in rhesus macaques. The hypothesis tested in the present study was that repeated administrations of a rhesusized anti-IL-15 monoclonal antibody would block IL-15 activity in vivo and result in changes to T and/or NK cell population dynamics that would reflect physiologic IL-15 function. The results provide important information on the specific role IL-15 plays in effector memory T cell and NK cell homeostasis, noting that effector memory T cells but not NK cells can be maintained in the absence of IL-15 signaling by the activity of other cytokines.
2016-09-07 | GSE76796 | GEO
Project description:Analysis of the effect of anti-IL-15 monoclonal antibody treatment on T cell and NK cell homeostasis in rhesus macaques. The hypothesis tested in the present study was that repeated administrations of a rhesusized anti-IL-15 monoclonal antibody would block IL-15 activity in vivo and result in changes to T and/or NK cell population dynamics that would reflect physiologic IL-15 function. The results provide important information on the specific role IL-15 plays in effector memory T cell and NK cell homeostasis, noting that effector memory T cells but not NK cells can be maintained in the absence of IL-15 signaling by the activity of other cytokines.
2016-09-07 | GSE76785 | GEO
Project description:NK cells are an essential component for the control of influenza infection, acting to both clear virus-infected cells and release antiviral cytokines. Engagement of the NK cell CD16-receptor by antibody-coated influenza-infected cells results in antibody-dependent cellular cytotoxicity (ADCC). Though NK cell-mediated ADCC is an important mechanism to control influenza, influenza infection itself may act to enhance the potency of NK cell ADCC. To understand if virus-infected cells increase NK cell activation, we co-cultured human PBMCs with influenza-infected human alveolar epithelial (A549) cells and evaluated the capacity of NK cells to mediate ADCC. Pre-incubation of PBMCs with influenza-infected target cells markedly enhanced the functionality of NK cells by ADCC antibodies in response to HA immune-complexes containing intravenous immunoglobulin (IVIG), allogenic target cells, with and without rituximab. Trans-well and supernatant transfer experiments showed that virus released into the supernatant is responsible for the enhanced functionality of NK cells, which is apparent at both the protein and RNA transcriptomic levels. Furthermore, cytokine multiplex data, RNA sequencing and cytokine blocking/supplementation experiments showed Type I interferons released from PBMCs were the primary mechanism of the influenza-induced increased NK cell functionality and ADCC potency. Importantly, the influenza infection-mediated increase in NK cell mediated anti-influenza ADCC was mimicked by the type I interferon agonist Poly-IC. This suggests a potential mechanism for enhancing monoclonal antibody therapies for influenza. We conclude that influenza-infection induced secretion of type I interferons enhances the ADCC capacity of NK cells and this pathway may potentially be manipulated to improve anti-influenza therapies.
2019-01-03 | GSE115203 | GEO
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Project description:We have developed a monoclonal antibody (mAb) C7 that reacts with Als3p and enolase present in Candida albicans cell wall and exerts three anti-Candida activities: candidacidal activity and inhibition of both adhesion and filamentation. To investigate the mode of action of mAb C7 on fungal viability, we examined changes in the genome-wide gene expression profile of C. albicans grown in presence of a subinhibitory concentration of mAb C7 (12.5 µg/ml) by using microarrays. A total of 49 genes were found to be differentially expressed upon treatment with mAb C7. Of these, 28 were found to be up-regulated and 21 down-regulated. The categories of up-regulated genes with the largest number of variations were those involved in iron uptake or related to iron homeostasis (42.86%), while the energy-related group accounted for 38.10% of the down-regulated genes (8/21). Results were validated by real Time PCR. Since these effects resembled those found under iron-limited conditions, the activity of mAb C7 on C. albicans mutants with deletions in key genes implicated in the three iron acquisition systems described in this yeast was also assessed. Only mutants lacking TPK1 and TPK2 genes were less sensitive to the candidacidal effect of mAb C7. FeCl3 or hemin at concentrations ≥ 7.8µM reversed the candidacidal effect of mAb C7 on C. albicans, on a concentration dependent manner. The results presented in this study provide evidence that the candidacidal effect of mAb C7 is related to the blockage of the reductive iron uptake pathway of C. albicans. A saturated culture of C. albicans grown overnight was diluted to an optical density at 600 nm of approximately 0.1 and divided in two aliquots. One of them was used untreated as control and the second one was treated with a subinhibitory concentration (12.5 µg/ml) of monoclonal antibody C7 . Both cultures were incubated for 18 h at 37ºC before harvesting cells. Antibody added and control samples were obtained each time. The experiment was repeated once. Dye-swap technique was used for hybridization and four arrays were analyzed to compare the expresion of over six thousands genes in response to antibody C7.
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