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Nanostring gene expresson-based, antibody activation of bone marrow derived macrophages (BMDM)

ABSTRACT: We study immune responses induced by amyloid targeting antibodies and CAA-mediated microhemorrhages using histology and gene expression analyses in AD mouse models and primary culture settings. We cultured and plated primary bone marrow-derived macrophages in wells coated with high Fc receptor activating antibody IgG2a or isotype control antibody harboring the LALAPG mutation, ablating Fc-FcR mediated effector functions

ORGANISM(S): Mus musculus

PROVIDER: GSE222466 | GEO | 2023/09/14

REPOSITORIES: GEO

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Expression data from Tbet+ and Tbet- Memory B cells

Project description:The role of antibody and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. Here we demonstrate that B cell specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells not only controlled IgG2a production, but also mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a since T-bet in B cells was important even in the presence of virus-specific IgG2a. Our data supports a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages. Naïve, Tbet+, and Tbet- Memory B cells were assayed for gene expression

2016-08-01 | GSE81189 | GEO

Expression data from Tbet+ and Tbet- Memory B cells

Project description:The role of antibody and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. Here we demonstrate that B cell specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells not only controlled IgG2a production, but also mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a since T-bet in B cells was imÂportant even in the presence of virus-specific IgG2a. Our data supports a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages. NaÃ¯ve, Tbet+, and Tbet- Memory B cells were assayed for gene expression Tbet GFP reporter mice were infected with LCMV clone 13, and target B cell populations were sorted from splenocytes at day 10 post-infection

2016-08-01 | E-GEOD-81189 | biostudies-arrayexpress

Global gene expression profiles of basophils isolated from human blood after engagement of immunoglobulins on their surface.

Project description:Basophils are blood leukocytes associated to Th2 responses and allergy reactions primarily through the IgE bound to their surface throught the Fc Epsilon hifh affinity receptor. Soluble IgD is an enigmatic antibody isotype whose function remains elusive. We have characterised the presence of this antibody isotype on the surface of basophils where we hypothesise that it plays a role in Th2 responses and allergy reactions.

2018-12-31 | GSE115296 | GEO

Comparative Analysis of Gene Expression in AgN2a-4P Expanded B6 NK Cells Treated with Anti-TIM-3 Antibody

Project description:Gene expression patterns in IL-15 or IL-15/AgN2a-4P expanded B6 NK cells treated with anti-TIM-3 antibody or IgG2a isotype control were analyzed using the nCounter Mouse PanCancer Immune Profiling Panel. Prior to RNA processing, NK cells were purified using the AutoMACS pro-separator (Miltenyi Biotec, San Jose, CA). The treatment involved a 4-hour exposure to antibodies before gene expression analysis, aiming to elucidate differential expression profiles in response to anti-TIM-3 treatment compared to the control condition.

2024-07-03 | GSE270965 | GEO

Bioinformatic analysis of PD-1 checkpoint blockade response in severe influenza infection [miRNA-Seq]

Project description:A BALB/c mouse model of severe influenza A/H1N1 infection was constructed, and whole-transcriptome sequencing of mice treated with PD-1 checkpoint blockade before severe A/PR8(H1N1) influenza infection and IgG2a isotype control before infection were performed.

2022-01-06 | GSE192915 | GEO

Bioinformatic analysis of PD-1 checkpoint blockade response in severe influenza infection [RNA-Seq]

2022-01-06 | GSE192914 | GEO

Frequent Evolution of Copy Number Alterations Following First‑line Treatment with FC(R) is Enriched with TP53 Alterations which Impact Long Term Survival – Results from the CLL8 Trial

Project description:To define clonal evolution of somatic copy number alterations (CNAs) in chronic lymphocytic leukemia (CLL), sequential samples of 103 individuals were investigated by SNP-array analysis for appearance of novel CNAs. Patients were enrolled on the CLL8 trial and uniformly received fludarabine, cyclophosphamide +/- rituximab (FC/FCR). Comparing two sequential samples prior to therapy (N=27, a median of 2.9 years apart), CNA evolution occurred in 19% of cases. In contrast, when comparing treatment‑initiation and relapse genomic profiles (a median of 3.6 years apart), CNA evolution was seen in 40% of cases. This suggested association of FC(R) treatment with higher rate of CNA evolution. The only clinical feature significantly associated with CNA evolution was FCR therapy compared with FC (OR=2.806, p=0.024). As this might be related to narrower evolutionary bottlenecks imposed by the more effective FCR therapy, which could execute more selection pressure, we examined matched minimal residual disease data. We found CNA evolution more frequently in cases with CLL cell numbers rapidly receding in early phases of treatment. Finally, we observed frequent rises of TP53 mutant/deficient clones with therapy (N=19, 22%) that were associated with decreased overall survival (p=0.016). These results demonstrated that re-examination of TP53 status upon relapse provides important information.

2017-08-25 | GSE83566 | GEO

Sequential gene expression profiling in CLL during treatment

Project description:Purpose: Accurate prediction of clinical response is the prerequisite for individualized therapy in chronic lymphocytic leukemia (CLL). We hypothesized that sequential assessment of gene expression changes early during therapy may well reflect behaviour of the leukemic clone in response to specific drugs. Patients and Methods: Gene expression profiles (GEP) were determined in CD19+ selected B-cells from 20 patients treated with fludarabine and cyclophosphamide (FC) (N=10) or FC plus rituximab (FCR) (N=10). Samples were collected in the first cycle before and within 48hours after initiation of treatment. GEP analysis was stratified by clinical response 3 months after start of therapy. Results: GEP before treatment detected high expression of 34 genes correlated with response and 32 genes correlated with resistance to therapy. These genes were related to regulation of apoptosis, cell cycle, cell adhesion, and signal transduction. Different results were obtained with sequential GEP: Sixteen genes were up-regulated after rituximab infusion in non-responders. Rituximab therapy resulted in down-regulation of AKT1 indicating involvement of the PI3-kinase pathway in CD20-signaling. Up-regulation of 24 genes after FC (including ITPKB (inositol 1,4,5-trisphosphate 3-kinase) and CD44) and of 36 genes after FCR (including CD49d) was associated with resistance. Down-regulation of CTLA4 correlated with poor response to FC. CD44, CD49d and the PI3-kinase signaling pathway were confirmed as potential therapeutic targets to overcome resistance by (protein analysis) or functional experiments. Conclusion Sequential GEP provides rapid and relevant information for prediction of response and resistance. This approach could be used to guide and adapt individualized therapy in CLL. 50 Samples from CD19 selected B-cells, three treatments (rituximab, FC and RFC), 10 replicates for each treatment, 20 replicates for control condition

2011-03-01 | E-GEOD-15490 | biostudies-arrayexpress

Untargeted lipidomics of liver to assess the potential protective role in atherosclerosis progression of A12 antibodies infusion into LDLR-/-mice

Project description:In order to assess the therapeutic potential of A12 antibodies in atherosclerosis, untargeted lipidomics of liver samples was performed. LDLR-/-mice were treated with a fully murine version of the A12 antibody (mA12-IgG2b), with the isotype control antibody mB1.8-IgG2b (n=16) or with PBS as controls.

2020-07-27 | ST001434 | MetabolomicsWorkbench

Expression data from T-cell Acute Lymphoblastic Leukemia (T-ALL) patient-derived xenograft treated with anti-CD3 mAbs.

Project description:T-cell acute lymphoblastic leukemia is an aggressive hematological malignancy treated with chemotherapy and has a poor prognosis. In previous studies, we demonstrated that T cell receptor (TCR)-induced negative selection is highly effective in combating T-ALL in mouse models. Moreover, targeting the TCR of diagnostic T-ALL-derived PDX with anti-hCD3 (aCD3) mAb OKT3 or the clinically relevant aCD3 mAb Teplizumab resulted in leukemic cell death, regression of leukemia, and improved host survival. The objective of the present experiment is to uncover the molecular mechanisms responsible for the anti-leukemic properties of the anti-CD3 mAbs OKT3 and Teplizumab in a T-ALL PDX model. We compare the transcriptomic profiles of FACS-sorted T-ALL cells extracted from T-ALL patient-derived xenograft (PDX) treated for 6h with isotype control antibody IgG2a or OKT3 mAb or Teplizumab mAb.

2024-03-19 | GSE240261 | GEO

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