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anti human cd22 antibody  (Boster Bio)


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    Boster Bio anti human cd22 antibody
    Anti Human Cd22 Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+human+cd22+antibody/Anti-CD22+%2F+BL-CAM+Monoclonal+Antibody/pm39528513-357-9-12
    Average 93 stars, based on 3 article reviews
    anti human cd22 antibody - by Bioz Stars, 2026-10
    93/100 stars

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    Western Blot:

    Article Title: Split-design approach enhances the therapeutic efficacy of ligand-based CAR-T cells against multiple B-cell malignancies
    Article Snippet: .. For western blot, anti-human CD19 antibody (Boster, BM4935) and anti-human CD22 antibody (Boster, BM4178) were used to verify the KO efficiency . .. Genes encoding the full-length BCMA antigen were synthesized by GenScript and cloned into the pLV lentiviral plasmid.

    Article Title: Split-design approach enhances the therapeutic efficacy of ligand-based CAR-T cells against multiple B-cell malignancies.
    Article Snippet: .. For western blot, antihuman CD19 antibody (Boster, BM4935) and anti-human CD22 antibody (Boster, BM4178) were used to verify the KO efficiency35. .. Generation of K562 cell variants with gradient expression of BCMA Genes encoding the full-length BCMA antigen were synthesized by GenScript and cloned into the pLV lentiviral plasmid.



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    MV-Blina therapy significantly prolongs the survival of ALL bearing mice (A) Treatment scheme. Two PDX models were established in NSG mice by i.v. injection to induce ALL. At a leukemic load of approximately 35%, mice received treatment i.v. with MV (2.5 × 10 5 TCID 50 /g) or control. Two days after infection, mice were injected with healthy human PBMCs. (B) Superior survival of PDX #2 with MV-Blina compared to MV-Edm. PDX #1 and #2 were treated either with MV-Blina and PBMC ( n = 10) or MV-Edm and PBMC ( n = 10) or control with PBMC only ( n = 10) and observed for a maximum of 70 days. (C) MV-Blina treatment decreases leukemic load. Leukemic blasts (msCD45 − huCD19 + huCD45 dim ) and human PBMC (msCD45 − huCD19 + huCD45 bright ) in peripheral blood were monitored by flow cytometry at the indicated time points. (D) Marked reduction of spleen weight in PDX upon MV-Blina treatment. At the time of death, a complete necropsy was performed, and spleen weight was determined. (E) Significant reduction of leukemic blasts by MV-Blina in ALL compartments. At the time of death, leukemic blasts (msCD45 − huCD19 + huCD45 dim ) were detected by flow cytometry in bone marrow, spleen, and meninges. Replication of secBlina was detected by qRT-PCR and calculated by the 2 −ΔΔCt method, displaying the fold change relative to huActin and huGAPDH. (F) MV-Blina reduces leukemic blasts in the spleen by decreasing proliferation and increasing apoptosis. Spleens of untreated mice at therapy start (d0, n = 4) and treated mice (MV-Blina and PBMC, n = 10; MV-Edm and PBMC, n = 9; PBMC-only control, n = 9) were formalin-fixed, paraffin-embedded, and subsequently stained for H&E, <t>CD22,</t> Ki67, or cleaved Caspase-3 (CC3). Positive area was determined using ImageJ. Scale bars 50 μm. Statistical analysis was performed using Mantel-Cox log rank test (B), one-way ANOVA with Tukey’s multiple comparisons test (C-F). ns, not significant; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; and ∗∗∗∗, p < 0.0001.
    Mouse Anti Human Cd22 Antibody, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    MV-Blina therapy significantly prolongs the survival of ALL bearing mice (A) Treatment scheme. Two PDX models were established in NSG mice by i.v. injection to induce ALL. At a leukemic load of approximately 35%, mice received treatment i.v. with MV (2.5 × 10 5 TCID 50 /g) or control. Two days after infection, mice were injected with healthy human PBMCs. (B) Superior survival of PDX #2 with MV-Blina compared to MV-Edm. PDX #1 and #2 were treated either with MV-Blina and PBMC ( n = 10) or MV-Edm and PBMC ( n = 10) or control with PBMC only ( n = 10) and observed for a maximum of 70 days. (C) MV-Blina treatment decreases leukemic load. Leukemic blasts (msCD45 − huCD19 + huCD45 dim ) and human PBMC (msCD45 − huCD19 + huCD45 bright ) in peripheral blood were monitored by flow cytometry at the indicated time points. (D) Marked reduction of spleen weight in PDX upon MV-Blina treatment. At the time of death, a complete necropsy was performed, and spleen weight was determined. (E) Significant reduction of leukemic blasts by MV-Blina in ALL compartments. At the time of death, leukemic blasts (msCD45 − huCD19 + huCD45 dim ) were detected by flow cytometry in bone marrow, spleen, and meninges. Replication of secBlina was detected by qRT-PCR and calculated by the 2 −ΔΔCt method, displaying the fold change relative to huActin and huGAPDH. (F) MV-Blina reduces leukemic blasts in the spleen by decreasing proliferation and increasing apoptosis. Spleens of untreated mice at therapy start (d0, n = 4) and treated mice (MV-Blina and PBMC, n = 10; MV-Edm and PBMC, n = 9; PBMC-only control, n = 9) were formalin-fixed, paraffin-embedded, and subsequently stained for H&E, <t>CD22,</t> Ki67, or cleaved Caspase-3 (CC3). Positive area was determined using ImageJ. Scale bars 50 μm. Statistical analysis was performed using Mantel-Cox log rank test (B), one-way ANOVA with Tukey’s multiple comparisons test (C-F). ns, not significant; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; and ∗∗∗∗, p < 0.0001.
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    MV-Blina therapy significantly prolongs the survival of ALL bearing mice (A) Treatment scheme. Two PDX models were established in NSG mice by i.v. injection to induce ALL. At a leukemic load of approximately 35%, mice received treatment i.v. with MV (2.5 × 10 5 TCID 50 /g) or control. Two days after infection, mice were injected with healthy human PBMCs. (B) Superior survival of PDX #2 with MV-Blina compared to MV-Edm. PDX #1 and #2 were treated either with MV-Blina and PBMC ( n = 10) or MV-Edm and PBMC ( n = 10) or control with PBMC only ( n = 10) and observed for a maximum of 70 days. (C) MV-Blina treatment decreases leukemic load. Leukemic blasts (msCD45 − huCD19 + huCD45 dim ) and human PBMC (msCD45 − huCD19 + huCD45 bright ) in peripheral blood were monitored by flow cytometry at the indicated time points. (D) Marked reduction of spleen weight in PDX upon MV-Blina treatment. At the time of death, a complete necropsy was performed, and spleen weight was determined. (E) Significant reduction of leukemic blasts by MV-Blina in ALL compartments. At the time of death, leukemic blasts (msCD45 − huCD19 + huCD45 dim ) were detected by flow cytometry in bone marrow, spleen, and meninges. Replication of secBlina was detected by qRT-PCR and calculated by the 2 −ΔΔCt method, displaying the fold change relative to huActin and huGAPDH. (F) MV-Blina reduces leukemic blasts in the spleen by decreasing proliferation and increasing apoptosis. Spleens of untreated mice at therapy start (d0, n = 4) and treated mice (MV-Blina and PBMC, n = 10; MV-Edm and PBMC, n = 9; PBMC-only control, n = 9) were formalin-fixed, paraffin-embedded, and subsequently stained for H&E, <t>CD22,</t> Ki67, or cleaved Caspase-3 (CC3). Positive area was determined using ImageJ. Scale bars 50 μm. Statistical analysis was performed using Mantel-Cox log rank test (B), one-way ANOVA with Tukey’s multiple comparisons test (C-F). ns, not significant; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; and ∗∗∗∗, p < 0.0001.
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    MV-Blina therapy significantly prolongs the survival of ALL bearing mice (A) Treatment scheme. Two PDX models were established in NSG mice by i.v. injection to induce ALL. At a leukemic load of approximately 35%, mice received treatment i.v. with MV (2.5 × 10 5 TCID 50 /g) or control. Two days after infection, mice were injected with healthy human PBMCs. (B) Superior survival of PDX #2 with MV-Blina compared to MV-Edm. PDX #1 and #2 were treated either with MV-Blina and PBMC ( n = 10) or MV-Edm and PBMC ( n = 10) or control with PBMC only ( n = 10) and observed for a maximum of 70 days. (C) MV-Blina treatment decreases leukemic load. Leukemic blasts (msCD45 − huCD19 + huCD45 dim ) and human PBMC (msCD45 − huCD19 + huCD45 bright ) in peripheral blood were monitored by flow cytometry at the indicated time points. (D) Marked reduction of spleen weight in PDX upon MV-Blina treatment. At the time of death, a complete necropsy was performed, and spleen weight was determined. (E) Significant reduction of leukemic blasts by MV-Blina in ALL compartments. At the time of death, leukemic blasts (msCD45 − huCD19 + huCD45 dim ) were detected by flow cytometry in bone marrow, spleen, and meninges. Replication of secBlina was detected by qRT-PCR and calculated by the 2 −ΔΔCt method, displaying the fold change relative to huActin and huGAPDH. (F) MV-Blina reduces leukemic blasts in the spleen by decreasing proliferation and increasing apoptosis. Spleens of untreated mice at therapy start (d0, n = 4) and treated mice (MV-Blina and PBMC, n = 10; MV-Edm and PBMC, n = 9; PBMC-only control, n = 9) were formalin-fixed, paraffin-embedded, and subsequently stained for H&E, <t>CD22,</t> Ki67, or cleaved Caspase-3 (CC3). Positive area was determined using ImageJ. Scale bars 50 μm. Statistical analysis was performed using Mantel-Cox log rank test (B), one-way ANOVA with Tukey’s multiple comparisons test (C-F). ns, not significant; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; and ∗∗∗∗, p < 0.0001.
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    Average 90 stars, based on 1 article reviews
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    90/100 stars
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    cd22  (Miltenyi Biotec)
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    MV-Blina therapy significantly prolongs the survival of ALL bearing mice (A) Treatment scheme. Two PDX models were established in NSG mice by i.v. injection to induce ALL. At a leukemic load of approximately 35%, mice received treatment i.v. with MV (2.5 × 10 5 TCID 50 /g) or control. Two days after infection, mice were injected with healthy human PBMCs. (B) Superior survival of PDX #2 with MV-Blina compared to MV-Edm. PDX #1 and #2 were treated either with MV-Blina and PBMC ( n = 10) or MV-Edm and PBMC ( n = 10) or control with PBMC only ( n = 10) and observed for a maximum of 70 days. (C) MV-Blina treatment decreases leukemic load. Leukemic blasts (msCD45 − huCD19 + huCD45 dim ) and human PBMC (msCD45 − huCD19 + huCD45 bright ) in peripheral blood were monitored by flow cytometry at the indicated time points. (D) Marked reduction of spleen weight in PDX upon MV-Blina treatment. At the time of death, a complete necropsy was performed, and spleen weight was determined. (E) Significant reduction of leukemic blasts by MV-Blina in ALL compartments. At the time of death, leukemic blasts (msCD45 − huCD19 + huCD45 dim ) were detected by flow cytometry in bone marrow, spleen, and meninges. Replication of secBlina was detected by qRT-PCR and calculated by the 2 −ΔΔCt method, displaying the fold change relative to huActin and huGAPDH. (F) MV-Blina reduces leukemic blasts in the spleen by decreasing proliferation and increasing apoptosis. Spleens of untreated mice at therapy start (d0, n = 4) and treated mice (MV-Blina and PBMC, n = 10; MV-Edm and PBMC, n = 9; PBMC-only control, n = 9) were formalin-fixed, paraffin-embedded, and subsequently stained for H&E, <t>CD22,</t> Ki67, or cleaved Caspase-3 (CC3). Positive area was determined using ImageJ. Scale bars 50 μm. Statistical analysis was performed using Mantel-Cox log rank test (B), one-way ANOVA with Tukey’s multiple comparisons test (C-F). ns, not significant; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; and ∗∗∗∗, p < 0.0001.
    Cd22, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti-human cd22-pe antibody  (STEMCELL Technologies Inc)
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    STEMCELL Technologies Inc anti-human cd22-pe antibody
    MV-Blina therapy significantly prolongs the survival of ALL bearing mice (A) Treatment scheme. Two PDX models were established in NSG mice by i.v. injection to induce ALL. At a leukemic load of approximately 35%, mice received treatment i.v. with MV (2.5 × 10 5 TCID 50 /g) or control. Two days after infection, mice were injected with healthy human PBMCs. (B) Superior survival of PDX #2 with MV-Blina compared to MV-Edm. PDX #1 and #2 were treated either with MV-Blina and PBMC ( n = 10) or MV-Edm and PBMC ( n = 10) or control with PBMC only ( n = 10) and observed for a maximum of 70 days. (C) MV-Blina treatment decreases leukemic load. Leukemic blasts (msCD45 − huCD19 + huCD45 dim ) and human PBMC (msCD45 − huCD19 + huCD45 bright ) in peripheral blood were monitored by flow cytometry at the indicated time points. (D) Marked reduction of spleen weight in PDX upon MV-Blina treatment. At the time of death, a complete necropsy was performed, and spleen weight was determined. (E) Significant reduction of leukemic blasts by MV-Blina in ALL compartments. At the time of death, leukemic blasts (msCD45 − huCD19 + huCD45 dim ) were detected by flow cytometry in bone marrow, spleen, and meninges. Replication of secBlina was detected by qRT-PCR and calculated by the 2 −ΔΔCt method, displaying the fold change relative to huActin and huGAPDH. (F) MV-Blina reduces leukemic blasts in the spleen by decreasing proliferation and increasing apoptosis. Spleens of untreated mice at therapy start (d0, n = 4) and treated mice (MV-Blina and PBMC, n = 10; MV-Edm and PBMC, n = 9; PBMC-only control, n = 9) were formalin-fixed, paraffin-embedded, and subsequently stained for H&E, <t>CD22,</t> Ki67, or cleaved Caspase-3 (CC3). Positive area was determined using ImageJ. Scale bars 50 μm. Statistical analysis was performed using Mantel-Cox log rank test (B), one-way ANOVA with Tukey’s multiple comparisons test (C-F). ns, not significant; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; and ∗∗∗∗, p < 0.0001.
    Anti Human Cd22 Pe Antibody, supplied by STEMCELL Technologies Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    MV-Blina therapy significantly prolongs the survival of ALL bearing mice (A) Treatment scheme. Two PDX models were established in NSG mice by i.v. injection to induce ALL. At a leukemic load of approximately 35%, mice received treatment i.v. with MV (2.5 × 10 5 TCID 50 /g) or control. Two days after infection, mice were injected with healthy human PBMCs. (B) Superior survival of PDX #2 with MV-Blina compared to MV-Edm. PDX #1 and #2 were treated either with MV-Blina and PBMC ( n = 10) or MV-Edm and PBMC ( n = 10) or control with PBMC only ( n = 10) and observed for a maximum of 70 days. (C) MV-Blina treatment decreases leukemic load. Leukemic blasts (msCD45 − huCD19 + huCD45 dim ) and human PBMC (msCD45 − huCD19 + huCD45 bright ) in peripheral blood were monitored by flow cytometry at the indicated time points. (D) Marked reduction of spleen weight in PDX upon MV-Blina treatment. At the time of death, a complete necropsy was performed, and spleen weight was determined. (E) Significant reduction of leukemic blasts by MV-Blina in ALL compartments. At the time of death, leukemic blasts (msCD45 − huCD19 + huCD45 dim ) were detected by flow cytometry in bone marrow, spleen, and meninges. Replication of secBlina was detected by qRT-PCR and calculated by the 2 −ΔΔCt method, displaying the fold change relative to huActin and huGAPDH. (F) MV-Blina reduces leukemic blasts in the spleen by decreasing proliferation and increasing apoptosis. Spleens of untreated mice at therapy start (d0, n = 4) and treated mice (MV-Blina and PBMC, n = 10; MV-Edm and PBMC, n = 9; PBMC-only control, n = 9) were formalin-fixed, paraffin-embedded, and subsequently stained for H&E, CD22, Ki67, or cleaved Caspase-3 (CC3). Positive area was determined using ImageJ. Scale bars 50 μm. Statistical analysis was performed using Mantel-Cox log rank test (B), one-way ANOVA with Tukey’s multiple comparisons test (C-F). ns, not significant; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; and ∗∗∗∗, p < 0.0001.

    Journal: Molecular Therapy Oncology

    Article Title: A measles virus encoding a CD19/CD3 bispecific T cell engager shows enhanced preclinical anti-BCP-ALL efficacy without significant toxicity

    doi: 10.1016/j.omton.2026.201127

    Figure Lengend Snippet: MV-Blina therapy significantly prolongs the survival of ALL bearing mice (A) Treatment scheme. Two PDX models were established in NSG mice by i.v. injection to induce ALL. At a leukemic load of approximately 35%, mice received treatment i.v. with MV (2.5 × 10 5 TCID 50 /g) or control. Two days after infection, mice were injected with healthy human PBMCs. (B) Superior survival of PDX #2 with MV-Blina compared to MV-Edm. PDX #1 and #2 were treated either with MV-Blina and PBMC ( n = 10) or MV-Edm and PBMC ( n = 10) or control with PBMC only ( n = 10) and observed for a maximum of 70 days. (C) MV-Blina treatment decreases leukemic load. Leukemic blasts (msCD45 − huCD19 + huCD45 dim ) and human PBMC (msCD45 − huCD19 + huCD45 bright ) in peripheral blood were monitored by flow cytometry at the indicated time points. (D) Marked reduction of spleen weight in PDX upon MV-Blina treatment. At the time of death, a complete necropsy was performed, and spleen weight was determined. (E) Significant reduction of leukemic blasts by MV-Blina in ALL compartments. At the time of death, leukemic blasts (msCD45 − huCD19 + huCD45 dim ) were detected by flow cytometry in bone marrow, spleen, and meninges. Replication of secBlina was detected by qRT-PCR and calculated by the 2 −ΔΔCt method, displaying the fold change relative to huActin and huGAPDH. (F) MV-Blina reduces leukemic blasts in the spleen by decreasing proliferation and increasing apoptosis. Spleens of untreated mice at therapy start (d0, n = 4) and treated mice (MV-Blina and PBMC, n = 10; MV-Edm and PBMC, n = 9; PBMC-only control, n = 9) were formalin-fixed, paraffin-embedded, and subsequently stained for H&E, CD22, Ki67, or cleaved Caspase-3 (CC3). Positive area was determined using ImageJ. Scale bars 50 μm. Statistical analysis was performed using Mantel-Cox log rank test (B), one-way ANOVA with Tukey’s multiple comparisons test (C-F). ns, not significant; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; and ∗∗∗∗, p < 0.0001.

    Article Snippet: Immunohistochemistry for CD22 was performed using a mouse anti-human CD22 antibody (clone OTI1F2, 1:75, TA506404, Origene, Rockville, MD), for Ki67 using a mouse anti-human Ki67 antibody (clone MIB-1, 1:150, M7240, Dako, Waldbronn, Germany) and for cleaved caspase-3 (CC3) using a rabbit-anti human active caspase-3 antibody (1:200, ab13847, Abcam, Cambridge, UK).

    Techniques: Injection, Control, Infection, Flow Cytometry, Quantitative RT-PCR, Formalin-fixed Paraffin-Embedded, Staining