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cpg b  (InvivoGen)


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    Structured Review

    InvivoGen cpg b
    Impaired CD4 and CD8 T cell priming is not due to inherent T cell-intrinsic defects in mice lacking VPS33B in DCs and other myeloid cells (A) Schematic of experimental set-up for adoptive T cell transfer and protein immunization. CD45.1 + OT-I and OT-II T cells were isolated and transferred into VPS33B WT and VPS33B ΔCSF1R mice. 24 h later, mice were immunized with 50 μg of OVA and 5 μg of LPS or 10 μg <t>of</t> <t>CpG-B</t> in IFA (100 μL/mouse; hock injection). 7 days later, IgLNs were collected and subject to flow cytometry. (B) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-II and OT-I cells from immunized LNs to the right. (C) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-I and OT-II cells from immunized LNs to the right. Error bars shown as mean ± SEM. n = 4–5 biological replicates for one independent experiment. Statistical analysis was performed by unpaired t test. ∗ p < . 05 , ∗∗ p < 0 . 01 , ∗∗∗p < 0 . 0001 , n.s. = not significant.
    Cpg B, supplied by InvivoGen, used in various techniques. Bioz Stars score: 97/100, based on 314 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cpg+odn+1668/pmc13223964-83-0-2?v=InvivoGen
    Average 97 stars, based on 314 article reviews
    cpg b - by Bioz Stars, 2026-07
    97/100 stars

    Images

    1) Product Images from "VPS33B regulates MHC class II antigen presentation in dendritic cells to drive CD4 T cell immunity"

    Article Title: VPS33B regulates MHC class II antigen presentation in dendritic cells to drive CD4 T cell immunity

    Journal: iScience

    doi: 10.1016/j.isci.2026.116052

    Impaired CD4 and CD8 T cell priming is not due to inherent T cell-intrinsic defects in mice lacking VPS33B in DCs and other myeloid cells (A) Schematic of experimental set-up for adoptive T cell transfer and protein immunization. CD45.1 + OT-I and OT-II T cells were isolated and transferred into VPS33B WT and VPS33B ΔCSF1R mice. 24 h later, mice were immunized with 50 μg of OVA and 5 μg of LPS or 10 μg of CpG-B in IFA (100 μL/mouse; hock injection). 7 days later, IgLNs were collected and subject to flow cytometry. (B) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-II and OT-I cells from immunized LNs to the right. (C) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-I and OT-II cells from immunized LNs to the right. Error bars shown as mean ± SEM. n = 4–5 biological replicates for one independent experiment. Statistical analysis was performed by unpaired t test. ∗ p < . 05 , ∗∗ p < 0 . 01 , ∗∗∗p < 0 . 0001 , n.s. = not significant.
    Figure Legend Snippet: Impaired CD4 and CD8 T cell priming is not due to inherent T cell-intrinsic defects in mice lacking VPS33B in DCs and other myeloid cells (A) Schematic of experimental set-up for adoptive T cell transfer and protein immunization. CD45.1 + OT-I and OT-II T cells were isolated and transferred into VPS33B WT and VPS33B ΔCSF1R mice. 24 h later, mice were immunized with 50 μg of OVA and 5 μg of LPS or 10 μg of CpG-B in IFA (100 μL/mouse; hock injection). 7 days later, IgLNs were collected and subject to flow cytometry. (B) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-II and OT-I cells from immunized LNs to the right. (C) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-I and OT-II cells from immunized LNs to the right. Error bars shown as mean ± SEM. n = 4–5 biological replicates for one independent experiment. Statistical analysis was performed by unpaired t test. ∗ p < . 05 , ∗∗ p < 0 . 01 , ∗∗∗p < 0 . 0001 , n.s. = not significant.

    Techniques Used: Isolation, Injection, Flow Cytometry



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    Impaired CD4 and CD8 T cell priming is not due to inherent T cell-intrinsic defects in mice lacking VPS33B in DCs and other myeloid cells (A) Schematic of experimental set-up for adoptive T cell transfer and protein immunization. CD45.1 + OT-I and OT-II T cells were isolated and transferred into VPS33B WT and VPS33B ΔCSF1R mice. 24 h later, mice were immunized with 50 μg of OVA and 5 μg of LPS or 10 μg <t>of</t> <t>CpG-B</t> in IFA (100 μL/mouse; hock injection). 7 days later, IgLNs were collected and subject to flow cytometry. (B) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-II and OT-I cells from immunized LNs to the right. (C) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-I and OT-II cells from immunized LNs to the right. Error bars shown as mean ± SEM. n = 4–5 biological replicates for one independent experiment. Statistical analysis was performed by unpaired t test. ∗ p < . 05 , ∗∗ p < 0 . 01 , ∗∗∗p < 0 . 0001 , n.s. = not significant.
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    Impaired CD4 and CD8 T cell priming is not due to inherent T cell-intrinsic defects in mice lacking VPS33B in DCs and other myeloid cells (A) Schematic of experimental set-up for adoptive T cell transfer and protein immunization. CD45.1 + OT-I and OT-II T cells were isolated and transferred into VPS33B WT and VPS33B ΔCSF1R mice. 24 h later, mice were immunized with 50 μg of OVA and 5 μg of LPS or 10 μg <t>of</t> <t>CpG-B</t> in IFA (100 μL/mouse; hock injection). 7 days later, IgLNs were collected and subject to flow cytometry. (B) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-II and OT-I cells from immunized LNs to the right. (C) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-I and OT-II cells from immunized LNs to the right. Error bars shown as mean ± SEM. n = 4–5 biological replicates for one independent experiment. Statistical analysis was performed by unpaired t test. ∗ p < . 05 , ∗∗ p < 0 . 01 , ∗∗∗p < 0 . 0001 , n.s. = not significant.
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    Impaired CD4 and CD8 T cell priming is not due to inherent T cell-intrinsic defects in mice lacking VPS33B in DCs and other myeloid cells (A) Schematic of experimental set-up for adoptive T cell transfer and protein immunization. CD45.1 + OT-I and OT-II T cells were isolated and transferred into VPS33B WT and VPS33B ΔCSF1R mice. 24 h later, mice were immunized with 50 μg of OVA and 5 μg of LPS or 10 μg <t>of</t> <t>CpG-B</t> in IFA (100 μL/mouse; hock injection). 7 days later, IgLNs were collected and subject to flow cytometry. (B) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-II and OT-I cells from immunized LNs to the right. (C) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-I and OT-II cells from immunized LNs to the right. Error bars shown as mean ± SEM. n = 4–5 biological replicates for one independent experiment. Statistical analysis was performed by unpaired t test. ∗ p < . 05 , ∗∗ p < 0 . 01 , ∗∗∗p < 0 . 0001 , n.s. = not significant.
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    Image Search Results


    Impaired CD4 and CD8 T cell priming is not due to inherent T cell-intrinsic defects in mice lacking VPS33B in DCs and other myeloid cells (A) Schematic of experimental set-up for adoptive T cell transfer and protein immunization. CD45.1 + OT-I and OT-II T cells were isolated and transferred into VPS33B WT and VPS33B ΔCSF1R mice. 24 h later, mice were immunized with 50 μg of OVA and 5 μg of LPS or 10 μg of CpG-B in IFA (100 μL/mouse; hock injection). 7 days later, IgLNs were collected and subject to flow cytometry. (B) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-II and OT-I cells from immunized LNs to the right. (C) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-I and OT-II cells from immunized LNs to the right. Error bars shown as mean ± SEM. n = 4–5 biological replicates for one independent experiment. Statistical analysis was performed by unpaired t test. ∗ p < . 05 , ∗∗ p < 0 . 01 , ∗∗∗p < 0 . 0001 , n.s. = not significant.

    Journal: iScience

    Article Title: VPS33B regulates MHC class II antigen presentation in dendritic cells to drive CD4 T cell immunity

    doi: 10.1016/j.isci.2026.116052

    Figure Lengend Snippet: Impaired CD4 and CD8 T cell priming is not due to inherent T cell-intrinsic defects in mice lacking VPS33B in DCs and other myeloid cells (A) Schematic of experimental set-up for adoptive T cell transfer and protein immunization. CD45.1 + OT-I and OT-II T cells were isolated and transferred into VPS33B WT and VPS33B ΔCSF1R mice. 24 h later, mice were immunized with 50 μg of OVA and 5 μg of LPS or 10 μg of CpG-B in IFA (100 μL/mouse; hock injection). 7 days later, IgLNs were collected and subject to flow cytometry. (B) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-II and OT-I cells from immunized LNs to the right. (C) Representative flow plots gating for transferred OT-I (live, CD90.2 + , Vα2 + , CD8 + , CD45.1 + ) or transferred OT-II (live, CD90.2 + , Vα2 + , CD8 − , CD45.1 + ) T cells. Pre-gated on live, CD90.2 + , Vα2 + cells. Quantification of % CD45.1 + , Vα2 + OT-I and OT-II cells from immunized LNs to the right. Error bars shown as mean ± SEM. n = 4–5 biological replicates for one independent experiment. Statistical analysis was performed by unpaired t test. ∗ p < . 05 , ∗∗ p < 0 . 01 , ∗∗∗p < 0 . 0001 , n.s. = not significant.

    Article Snippet: CpG-B , Invivogen , Cat#Tlrl-1668.

    Techniques: Isolation, Injection, Flow Cytometry