Odn2088

Manufactured by InvivoGen

Sourced in United States

ODN2088 is a synthetic oligodeoxynucleotide (ODN) containing the 2088 motif. It is designed for use in research applications.

Automatically generated - may contain errors

Lab products found in correlation

Anti hmgb1 antibody, by Abcam (3 mentions) Wild type c57bl 6 mice, by Jackson ImmunoResearch (3 mentions) Oligodeoxynucleotides odn 1826, by InvivoGen (3 mentions) Ifnα and ifnβ antibodies, by Thermo Fisher Scientific (3 mentions) Tlr9 mice, by Jackson ImmunoResearch (3 mentions) Odn 2088 control, by InvivoGen (3 mentions) Odn 2088 negative, by InvivoGen (2 mentions) Cl amidine, by Merck Group (2 mentions) Odn1668, by InvivoGen (2 mentions) Bafilomycin a1, by Merck Group (2 mentions) Lfm a13, by Merck Group (2 mentions) Sch772984, by Selleck Chemicals (1 mentions) Myd88, by Jackson ImmunoResearch (1 mentions) Stinggt gt, by Jackson ImmunoResearch (1 mentions) C57bl 6, by Jackson ImmunoResearch (1 mentions) Bio plex kit, by Bio-Rad (1 mentions) Poly 1 c, by InvivoGen (1 mentions) αtlr2, by InvivoGen (1 mentions) Odn1826, by InvivoGen (1 mentions) Ficoll paque plus gradient, by GE Healthcare (1 mentions)

35 protocols using odn2088

Investigating TLR9 Knockout in Mice

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C57BL/6 wild type (WT) mice and TLR9 -/-mice (male, aged 9-14 weeks, purchased from The Jackson Laboratory, Bar Harbor, ME) were used in the study. HCQ was purchased from ThermoFisher.
Oligodeoxynucleotides (ODN)-1826, ODN-2088, and ODN-2088 negative control were purchased from InvivoGen. Anti-HMGB1 antibodies were purchased from Abcam. IFNα and IFNβ antibodies were purchased from ThermoFisher.

Marsh K., Rastogi R., Zhang A., Wu D., Kron I.L., & Yang Z. (2021). Hydroxychloroquine Attenuates Myocardial Ischemic and Post-ischemic Reperfusion Injury by Inhibiting the Toll-like Receptor 9 – Type I Interferon Pathway.

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Modulation of Fibroblast-Macrophage Crosstalk

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Term human FM explants were collected as described above, rested in DMEM/F12 media supplemented with 10% FBS overnight and then treated with neutrophil CM for 24 hrs. In some experiments, FMs were pre-treated with the ERK inhibitor, SCH772984 (10nM, Selleckchem, Houston, TX); or the TLR9 antagonist, ODN2088 (TTAGGG, 1μM, Invivogen, A151, San Diego, CA) for 1 hr at 37°C prior to the addition of neutrophil CM. In other cases, DNase I derived from bovine pancreas (1U/ml, Roche, #10104159001, Roche, Switizerland) was added to neutrophil CM for 30 min at room temperature then the CM incubated at 70°C for 20 min and cooled prior to adding to the FMs. Neutrophil CM was incubated at 70°C for 20 min without DNase I as the baseline control. Incubation of activated neutrophil CM at 70°C for 20 min without DNase I did not affect its ability to alter FM function. After 24 hr of co-culture, the neutrophil CM and any associated factors was removed and FMs were transferred to a serum-free OptiMEM culture system for an additional 24 hrs to collect freshly secreted FM-derived factors for downstream analysis. FM supernatants and tissues are collected and stored at −80°C until analysis.

Tong M., Smith A.H, & Abrahams V.M. (2021). Activated Neutrophils Propagate Fetal Membrane Inflammation and Weakening through ERK and Neutrophil Extracellular Trap-induced TLR-9 Signaling. Journal of immunology (Baltimore, Md. : 1950), 206(5), 1039-1045.

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Immune Signaling Pathways in Murine Studies

Cited 1 time

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Wild-type (WT) C57BL/6, TLR2^−/−, MyD88^−/−, μMT, and STING^gt/gt mice were purchased from The Jackson Laboratory. TLR9^−/− mice had been kindly provided by Dr. Daniel Muruve (University of Calgary) and were bred in house at the University of Florida [18 (link)]. IFNαR^−/− mice were housed at Baylor College of Medicine as previously described [23 (link)]. All knockout mice were on a C57BL/6 background. Animals were housed under specific pathogen free conditions at the University of Florida or Baylor College of Medicine and treated under Institutional Animal Care and Use Committee approved protocols. All animals were male and 6-8 weeks old at the onset of the experiments; all cohorts contained at least 4 mice per group.
AAV vectors were administered intramuscularly or intravenously as previously described [18 (link),20 (link)]. Plasma samples were collected by retro-orbital bleed into heparinized capillary tubes. TLR9i (ODN 2088, Invivogen) was delivered at 100 μg/mouse mixed with the vector formulation as previously described [18 (link)]. MyD88 inhibitor (MyD88i) and control peptide (MyD88c) (IMG-2005, Imgenex) were delivered at 25 μg/mouse i.p. in 100 μL PBS as previously described [24 (link)].

Rogers G.L., Suzuki M., Zolotukhin I., Markusic D.M., Morel L.M., Lee B., Ertl H.C, & Herzog R.W. (2015). Unique Roles of TLR9- and MyD88-Dependent and -Independent Pathways in Adaptive Immune Responses to AAV-Mediated Gene Transfer. Journal of Innate Immunity, 7(3), 302-314.

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Anti-Tularemia LPS Monoclonal Antibody Protocol

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Anti-F. tularensis LPS monoclonal antibody (mouse IgG2a) was purchased from Fitzgerald Industries (Acton, MA). Lipopolysaccharide from E. coli O111:B4 (LPS) was purchased from Millipore Sigma, (Burlington, MA). Poly(I:C), a TLR3 ligand; ODN 1826, a TLR9 agonist; ODN 2088, a TLR9 antagonist; and R406, a Syk inhibitor, were purchased from InvivoGen (San Diego, CA). Bio-Plex® kits were purchased from Bio-Rad (Hercules, CA). eFluor 450 conjugated anti-MHC Class II (I-A/I-E) Monoclonal Antibody (clone M5/114.15.2) was purchased from eBioscience (Waltham, MA). PE conjugated anti-CD80 Antibody (clone 16–10A1) and APC conjugated anti-CD86Antibody (clone Gl-1) were purchased from BioLegend (San Diego, CA). αTLR2 was purchased from InvivoGen. αFcγRI clone # 290322 was purchased from R&D Systems. αFcγRII/III (Mouse BD Fc Block) clone 2.4G2 was purchased from BD Biosciences (San Jose, CA). Mouse IgG2a Isotype Control clone UPC-10 for making mAb-beads was purchased from Millipore Sigma.

Nelson N.L., Hanes C.M., Lennartz M.R, & Gosselin E.J. (2019). Fcγ receptors and toll-like receptor 9 synergize to drive immune complex-induced dendritic cell maturation.. Cellular immunology, 345, 103962.

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Toll-like Receptor 9 Modulation in Embryo

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Previous studies tested various oligonucleotides (ODNs) for their stimulatory or inhibitory activities for Toll-like receptor 9 (TLR9; Krieg et al., 1995 (link); Stunz et al., 2002 (link)). Based on the finding that ODN 2088 is one of the most effective inhibitors, we applied it in our experiments as TLR9 antagonist. The ODN 2088 (5'-TCC TGG CGG GGA AGT-3') was purchased from Invivogen. The drug was suspended in endotoxin-free water and dissolved in plasmid DNA solution at a mass ratio of plasmid DNA/ODN 2088 1:1. Plasmid DNA and ODN 2088 were injected into the lateral ventricles of E12 embryos. After 2 d (E14), the brains were perfused with 4% PFA and subjected to immunohistochemistry.

Hattori Y, & Miyata T. (2018). Embryonic Neocortical Microglia Express Toll-Like Receptor 9 and Respond to Plasmid DNA Injected into the Ventricle: Technical Considerations Regarding Microglial Distribution in Electroporated Brain Walls. eNeuro, 5(6), ENEURO.0312-18.2018.

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Exosome-induced PBMC Cytokine Response

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Peripheral blood mononuclear cells (PBMCs) were isolated from heparinzed peripheral venous blood of HCs by density gradient centrifugation using Ficoll-paque plus gradient (GE Healthcare Biosciences, Uppsala, Sweden). Cell viability was assessed with trypan blue dye exclusion. PBMCs (5 × 10⁶ cells/mL) were stimulated with 10 μL purified exosomes in RPMI-1640 supplemented with 100 U/mL penicillin and 100 μL/mL streptomycin for 24 h at 37 °C in a 5 % CO₂ incubator.
To investigate the involvement of TLRs, PBMCs were pretreated with TLR1/2 antagonist (CU-CPT22; Calbiochem, MA, USA), TLR4 antagonist (LPS-RS ultrapure; Invivogen, CA, USA), TLR7 antagonist (ODN20958; Invivogen, CA, USA), or TLR9 antagonist (ODN2088; Invivogen, CA, USA) for 1 h. Then the cells were incubated with exosomes for 24 h. Following stimulation, levels of IFN-α, TNF-α, IL-1β, and IL-6 in the supernatants were measured using ELISA according to the manufacturers’ instructions (IFN-α, PBL Assay Science, NJ, USA; TNF-α, IL-1β, and IL-6, BD Biosciences, CA, USA).

Lee J.Y., Park J.K., Lee E.Y., Lee E.B, & Song Y.W. (2016). Circulating exosomes from patients with systemic lupus erythematosus induce an proinflammatory immune response. Arthritis Research & Therapy, 18, 264.

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Synthesis and Functionalization of Gold Nanoparticles

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Chloroauric acid, tri-sodium citrate dihydrate (sodium citrate), tris(2-carboxyethyl)phosphine hydrochloride (TCEP), potassium iodide, iodine, 11-mercaptoundecyl hexa(ethylene glycol) (MUHEG), sodium borohydride, monosodium phosphate, dithiothreitol, hydrochloric acid (37%), and nitric acid (70%) were bought from Sigma Aldrich, St. Louis, MO. 15-nm AuNPs were synthesized by citrate reduction of Chloroauric acid following a previous protocol.³² CpG ODN (5’-TCCATGACGTTCCTGACGTT-(sp18)-disulfide-3’, phosphodiester backbone) and GpC ODN (5’-TCCATGAGCTTCCTGAGCTT-(sp18)-disulfide-3’, phosphodiester backbone) were synthesized by solid phase. Zeocin, Primocin, and antagonists for TLR7/8 (ODN 2087) and TLR7/8 and 9 (ODN 2088) were obtained from Invivogen, San Diego, CA. Fetal bovine serum (FBS), Dulbecco’s phosphate-buffered saline (DPBS) and Dulbecco’s Modified Eagle’s medium (DMEM) were purchased from Thermo Fisher Scientific, Waltham, MA.

Pallares R.M., Choo P., Cole L.E., Mirkin C.A., Lee A, & Odom T.W. (2019). Manipulating Immune Activation of Macrophages by Tuning the Oligonucleotide Composition of Gold Nanoparticles. Bioconjugate chemistry, 30(7), 2032-2037.

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Pristane-Induced Hybridoma Characterization and Antibody Purification

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The hybridoma clones PL2-3 (anti-chromatin IgG2a^a), PL2-8 (anti-chromatin IgG2b), Hy1.2 (anti-TNP IgG2a^a) and C4010 (anti-TNP IgG2a^b) have been previously described (9 (link)). Two months old mice were first injected i.p. with 250 ul of pristane (Sigma) on d0 and d7, then with 10⁷ hybridoma cells on d10, and sacrificed on d17. For TLR9 inhibition studies, 100 ug of the TLR9 inhibitor ODN 2088 (Invivogen) was co-injected with the hybridoma cells. This dose of TLR9 inhibitor was sufficient to suppress a humoral immune response for up to 4 weeks (29 (link)). Other mice were immunized i.p. with 1 mg/ml of purified PL2-3 Ab on d10, d12, and d15 following pristane injection and sacrificed on d18. To obtain purified PL2-3 Ab, BALB/c.Rag2^−/− mice were injected with 200 ul pristane and 10⁷ hybridoma cells 5 d later. The mice were euthanized when their body weight had increased by 15 %. Ascitic fluid was spun down and the supernatant was filtered using a 0.45 μm SFCA syringe filter (Corning). Purified PL2-3 antibody was quantified in Immulon 2 plates coated with 5 ug/ml rat anti-mouse IgG2a (BD Pharmingen). Both samples and mouse IgG2a standard (Southern Biotech) were serially diluted threefold and goat anti-mouse IgG2a-AP (Southern Biotech) was used as the secondary Ab.

Sang A., Niu H., Cullen J., Choi S.C., Zheng Y.Y., Wang H., Shlomchik M.J, & Morel L. (2014). Activation of rheumatoid factor-specific B cells is antigen-dependent and occurs preferentially outside of germinal centers in the lupus-prone NZM2410 mouse model. Journal of immunology (Baltimore, Md. : 1950), 193(4), 1609-1621.

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Pharmacological Modulation of Inflammatory Pathways in CLP Rats

Cited 2 times

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The CLP rats were injected with 150 ng/g ODN2088 (agonist of TLR9, InvivoGen, San Diego, CA, USA), 50 ng/g SB203580 (inhibitor of p38 MApK, Cell Signaling Technology, Beverly, MA, USA), 75 ng/g PD98059 (inhibitor of ERK, Cell Signaling Technology), 150 ng/g SP600125 (inhibitor of JNK, Cell Signaling Technology), 100 ng/g Z-DEVD-FMK (inhibitor of apoptosis, Selleck, Houston, TX, USA), 12.5 ng/g INF39 (inhibitor of pyroptosis, Selleck), 37.5 ng/g Nec-1s (inhibitor of necroptosis, Cell Signaling Technology), and 1% dimethyl sulfoxide (DMSO) (vehicle, Sigma-Aldrich, St. Louis, MO, USA).^{[22 (link)–28 (link)]}

Zhou R., Ying J., Qiu X., Yu L., Yue Y., Liu Q., Shi J., Li X., Qu Y, & Mu D. (2022). A new cell death program regulated by toll-like receptor 9 through p38 mitogen-activated protein kinase signaling pathway in a neonatal rat model with sepsis associated encephalopathy. Chinese Medical Journal, 135(12), 1474-1485.

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Murine B Cell Stimulation Assay

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Purified B cells (2 × 10⁶) from 6-8-week-old wild type B6 mice were stimulated with 2 μg/ml TLR9 antagonist (ODN2088, Invivogen), ODN 2088 control (Invivogen) or 10μM dexamethasone at 37 °C, 5% CO₂ for 12 h.

Wang P., Yang X., Zhang L., Sha S., Huang J., Peng J., Gu J., Pearson J.A., Hu Y., Zhao H., Wong F.S., Wang Q, & Wen L. (2024). Tlr9 deficiency in B cells leads to obesity by promoting inflammation and gut dysbiosis. Nature Communications, 15, 4232.

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