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anti cd22  (R&D Systems)


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    Structured Review

    R&D Systems anti cd22
    The ITAM-bearing Dectin-1 ( Clec7a ) was cloned from C57BL/6 mice and tagged with V5. Clec7a -V5 was overexpressed in HEK293T cells along with either vector control, <t>CD22</t> WT , or CD22 R130A . ( a ) Proximity ligation assay (PLA) <t>using</t> <t>anti-CD22</t> and anti-V5 antibodies revealed molecular proximity between Clec7a -V5 and CD22 WT or CD22 R130A . Data are presented as mean ± SEM (n = 3 independent replicates). Overexpression of Clec7a -V5 in HEK293T cells enabled the uptake of pHRodo red Zymosan bioparticles, and co-expression of CD22 WT or CD22 R130A ( b ) significantly suppressed this uptake, while co-expression of CD22 Y783/843/863F ( c ) did not. Data are presented as mean ± SEM (n = 3 independent replicates). ** p < 0.01, *** p < 0.001 and **** p < 0.0001 by one-way ANOVA. Scale bar = 10 µm.
    Anti Cd22, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti cd22/product/R&D Systems
    Average 94 stars, based on 1 article reviews
    anti cd22 - by Bioz Stars, 2026-05
    94/100 stars

    Images

    1) Product Images from "Oxidative Stress-Induced Microglial CD22 Upregulation Impairs Phagocytosis and Exacerbates Huntington’s Disease"

    Article Title: Oxidative Stress-Induced Microglial CD22 Upregulation Impairs Phagocytosis and Exacerbates Huntington’s Disease

    Journal: bioRxiv

    doi: 10.64898/2026.03.11.710967

    The ITAM-bearing Dectin-1 ( Clec7a ) was cloned from C57BL/6 mice and tagged with V5. Clec7a -V5 was overexpressed in HEK293T cells along with either vector control, CD22 WT , or CD22 R130A . ( a ) Proximity ligation assay (PLA) using anti-CD22 and anti-V5 antibodies revealed molecular proximity between Clec7a -V5 and CD22 WT or CD22 R130A . Data are presented as mean ± SEM (n = 3 independent replicates). Overexpression of Clec7a -V5 in HEK293T cells enabled the uptake of pHRodo red Zymosan bioparticles, and co-expression of CD22 WT or CD22 R130A ( b ) significantly suppressed this uptake, while co-expression of CD22 Y783/843/863F ( c ) did not. Data are presented as mean ± SEM (n = 3 independent replicates). ** p < 0.01, *** p < 0.001 and **** p < 0.0001 by one-way ANOVA. Scale bar = 10 µm.
    Figure Legend Snippet: The ITAM-bearing Dectin-1 ( Clec7a ) was cloned from C57BL/6 mice and tagged with V5. Clec7a -V5 was overexpressed in HEK293T cells along with either vector control, CD22 WT , or CD22 R130A . ( a ) Proximity ligation assay (PLA) using anti-CD22 and anti-V5 antibodies revealed molecular proximity between Clec7a -V5 and CD22 WT or CD22 R130A . Data are presented as mean ± SEM (n = 3 independent replicates). Overexpression of Clec7a -V5 in HEK293T cells enabled the uptake of pHRodo red Zymosan bioparticles, and co-expression of CD22 WT or CD22 R130A ( b ) significantly suppressed this uptake, while co-expression of CD22 Y783/843/863F ( c ) did not. Data are presented as mean ± SEM (n = 3 independent replicates). ** p < 0.01, *** p < 0.001 and **** p < 0.0001 by one-way ANOVA. Scale bar = 10 µm.

    Techniques Used: Clone Assay, Plasmid Preparation, Control, Proximity Ligation Assay, Over Expression, Expressing

    BV2-CD22 microglia were treated with either IgG isotype control or anti-CD22 antibody (Cy34.1) for 24 hours. ( a ) Immunofluorescence staining showed colocalization of CD22 (red) and Cy34.1 (grey) puncta (yellow arrows) within the cells. ( b ) Quantification of GFP showed that cells treated with IgG or Cy34.1 had comparable levels of CD22-GFP, while treatment with Cy34.1 reduced the overall amount of CD22. ( c ) Flow cytometry analysis confirmed similar CD22⁺ percentages (∼99.8%) across groups, but treatment with Cy34.1 reduced the amount of CD22 on the cell surface, as reflected by MFI. Data are presented as mean ± SEM (n = 3). ( d ) Phagocytosis of pHRodo red Zymosan particles was restored in BV2-CD22 cells treated with Cy34.1. Data are presented as mean ± SEM (n = 4 independent experiments). ( e-f ) Phagocytosis of pHRodo-labeled myelin debris was assessed in BV2-CD22 cells treated with Cy34.1 and neonatal primary microglia derived from wild-type (CD22 WT ) or CD22-knockout (CD22 KO ) mice. Phagocytic index was quantified as the percentage of pHRodo⁺ among CD11b⁺ microglia. Data are presented as mean ± SEM (n = 4-5 biological replicates). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 by unpaired t -test. Scale bar = 10 µm.
    Figure Legend Snippet: BV2-CD22 microglia were treated with either IgG isotype control or anti-CD22 antibody (Cy34.1) for 24 hours. ( a ) Immunofluorescence staining showed colocalization of CD22 (red) and Cy34.1 (grey) puncta (yellow arrows) within the cells. ( b ) Quantification of GFP showed that cells treated with IgG or Cy34.1 had comparable levels of CD22-GFP, while treatment with Cy34.1 reduced the overall amount of CD22. ( c ) Flow cytometry analysis confirmed similar CD22⁺ percentages (∼99.8%) across groups, but treatment with Cy34.1 reduced the amount of CD22 on the cell surface, as reflected by MFI. Data are presented as mean ± SEM (n = 3). ( d ) Phagocytosis of pHRodo red Zymosan particles was restored in BV2-CD22 cells treated with Cy34.1. Data are presented as mean ± SEM (n = 4 independent experiments). ( e-f ) Phagocytosis of pHRodo-labeled myelin debris was assessed in BV2-CD22 cells treated with Cy34.1 and neonatal primary microglia derived from wild-type (CD22 WT ) or CD22-knockout (CD22 KO ) mice. Phagocytic index was quantified as the percentage of pHRodo⁺ among CD11b⁺ microglia. Data are presented as mean ± SEM (n = 4-5 biological replicates). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 by unpaired t -test. Scale bar = 10 µm.

    Techniques Used: Control, Immunofluorescence, Staining, Flow Cytometry, Labeling, Derivative Assay, Knock-Out



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    The ITAM-bearing Dectin-1 ( Clec7a ) was cloned from C57BL/6 mice and tagged with V5. Clec7a -V5 was overexpressed in HEK293T cells along with either vector control, <t>CD22</t> WT , or CD22 R130A . ( a ) Proximity ligation assay (PLA) <t>using</t> <t>anti-CD22</t> and anti-V5 antibodies revealed molecular proximity between Clec7a -V5 and CD22 WT or CD22 R130A . Data are presented as mean ± SEM (n = 3 independent replicates). Overexpression of Clec7a -V5 in HEK293T cells enabled the uptake of pHRodo red Zymosan bioparticles, and co-expression of CD22 WT or CD22 R130A ( b ) significantly suppressed this uptake, while co-expression of CD22 Y783/843/863F ( c ) did not. Data are presented as mean ± SEM (n = 3 independent replicates). ** p < 0.01, *** p < 0.001 and **** p < 0.0001 by one-way ANOVA. Scale bar = 10 µm.
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    Immune cell abundance and phenotype undergone significant alterations in diabetic PAAD. A Immune score and abundance of dendritic cells, B cells, and CD8 + T cells by xCell. B Expression level of immune-exhaustion markers in tumor samples of non-diabetic and diabetic PAAD patients. C Pearson correlation analyses between the expression of immune-exhaustion genes and immune cell markers. Pink and red circles indicate R value 0.3–0.8 and > 0.8, respectively. D Single cell type specificity of <t>CD22</t> and TIGIT and their specific expression in bone marrow and lymph node immune cells from human single cell atlas
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    Image Search Results


    The ITAM-bearing Dectin-1 ( Clec7a ) was cloned from C57BL/6 mice and tagged with V5. Clec7a -V5 was overexpressed in HEK293T cells along with either vector control, CD22 WT , or CD22 R130A . ( a ) Proximity ligation assay (PLA) using anti-CD22 and anti-V5 antibodies revealed molecular proximity between Clec7a -V5 and CD22 WT or CD22 R130A . Data are presented as mean ± SEM (n = 3 independent replicates). Overexpression of Clec7a -V5 in HEK293T cells enabled the uptake of pHRodo red Zymosan bioparticles, and co-expression of CD22 WT or CD22 R130A ( b ) significantly suppressed this uptake, while co-expression of CD22 Y783/843/863F ( c ) did not. Data are presented as mean ± SEM (n = 3 independent replicates). ** p < 0.01, *** p < 0.001 and **** p < 0.0001 by one-way ANOVA. Scale bar = 10 µm.

    Journal: bioRxiv

    Article Title: Oxidative Stress-Induced Microglial CD22 Upregulation Impairs Phagocytosis and Exacerbates Huntington’s Disease

    doi: 10.64898/2026.03.11.710967

    Figure Lengend Snippet: The ITAM-bearing Dectin-1 ( Clec7a ) was cloned from C57BL/6 mice and tagged with V5. Clec7a -V5 was overexpressed in HEK293T cells along with either vector control, CD22 WT , or CD22 R130A . ( a ) Proximity ligation assay (PLA) using anti-CD22 and anti-V5 antibodies revealed molecular proximity between Clec7a -V5 and CD22 WT or CD22 R130A . Data are presented as mean ± SEM (n = 3 independent replicates). Overexpression of Clec7a -V5 in HEK293T cells enabled the uptake of pHRodo red Zymosan bioparticles, and co-expression of CD22 WT or CD22 R130A ( b ) significantly suppressed this uptake, while co-expression of CD22 Y783/843/863F ( c ) did not. Data are presented as mean ± SEM (n = 3 independent replicates). ** p < 0.01, *** p < 0.001 and **** p < 0.0001 by one-way ANOVA. Scale bar = 10 µm.

    Article Snippet: After blocking with 4% BSA for 1 hour at room temperature, samples were incubated with anti-CD22 (R&D Systems; AF2296) and anti-V5 (Invitrogen; SV5-Pk1) overnight at 4 °C in a humidified chamber.

    Techniques: Clone Assay, Plasmid Preparation, Control, Proximity Ligation Assay, Over Expression, Expressing

    BV2-CD22 microglia were treated with either IgG isotype control or anti-CD22 antibody (Cy34.1) for 24 hours. ( a ) Immunofluorescence staining showed colocalization of CD22 (red) and Cy34.1 (grey) puncta (yellow arrows) within the cells. ( b ) Quantification of GFP showed that cells treated with IgG or Cy34.1 had comparable levels of CD22-GFP, while treatment with Cy34.1 reduced the overall amount of CD22. ( c ) Flow cytometry analysis confirmed similar CD22⁺ percentages (∼99.8%) across groups, but treatment with Cy34.1 reduced the amount of CD22 on the cell surface, as reflected by MFI. Data are presented as mean ± SEM (n = 3). ( d ) Phagocytosis of pHRodo red Zymosan particles was restored in BV2-CD22 cells treated with Cy34.1. Data are presented as mean ± SEM (n = 4 independent experiments). ( e-f ) Phagocytosis of pHRodo-labeled myelin debris was assessed in BV2-CD22 cells treated with Cy34.1 and neonatal primary microglia derived from wild-type (CD22 WT ) or CD22-knockout (CD22 KO ) mice. Phagocytic index was quantified as the percentage of pHRodo⁺ among CD11b⁺ microglia. Data are presented as mean ± SEM (n = 4-5 biological replicates). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 by unpaired t -test. Scale bar = 10 µm.

    Journal: bioRxiv

    Article Title: Oxidative Stress-Induced Microglial CD22 Upregulation Impairs Phagocytosis and Exacerbates Huntington’s Disease

    doi: 10.64898/2026.03.11.710967

    Figure Lengend Snippet: BV2-CD22 microglia were treated with either IgG isotype control or anti-CD22 antibody (Cy34.1) for 24 hours. ( a ) Immunofluorescence staining showed colocalization of CD22 (red) and Cy34.1 (grey) puncta (yellow arrows) within the cells. ( b ) Quantification of GFP showed that cells treated with IgG or Cy34.1 had comparable levels of CD22-GFP, while treatment with Cy34.1 reduced the overall amount of CD22. ( c ) Flow cytometry analysis confirmed similar CD22⁺ percentages (∼99.8%) across groups, but treatment with Cy34.1 reduced the amount of CD22 on the cell surface, as reflected by MFI. Data are presented as mean ± SEM (n = 3). ( d ) Phagocytosis of pHRodo red Zymosan particles was restored in BV2-CD22 cells treated with Cy34.1. Data are presented as mean ± SEM (n = 4 independent experiments). ( e-f ) Phagocytosis of pHRodo-labeled myelin debris was assessed in BV2-CD22 cells treated with Cy34.1 and neonatal primary microglia derived from wild-type (CD22 WT ) or CD22-knockout (CD22 KO ) mice. Phagocytic index was quantified as the percentage of pHRodo⁺ among CD11b⁺ microglia. Data are presented as mean ± SEM (n = 4-5 biological replicates). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 by unpaired t -test. Scale bar = 10 µm.

    Article Snippet: After blocking with 4% BSA for 1 hour at room temperature, samples were incubated with anti-CD22 (R&D Systems; AF2296) and anti-V5 (Invitrogen; SV5-Pk1) overnight at 4 °C in a humidified chamber.

    Techniques: Control, Immunofluorescence, Staining, Flow Cytometry, Labeling, Derivative Assay, Knock-Out

    Immune cell abundance and phenotype undergone significant alterations in diabetic PAAD. A Immune score and abundance of dendritic cells, B cells, and CD8 + T cells by xCell. B Expression level of immune-exhaustion markers in tumor samples of non-diabetic and diabetic PAAD patients. C Pearson correlation analyses between the expression of immune-exhaustion genes and immune cell markers. Pink and red circles indicate R value 0.3–0.8 and > 0.8, respectively. D Single cell type specificity of CD22 and TIGIT and their specific expression in bone marrow and lymph node immune cells from human single cell atlas

    Journal: Cellular Oncology (Dordrecht, Netherlands)

    Article Title: CXCL12 derived from cancer-associated fibroblasts mediates dysfunctional intratumoral adaptive immunity in diabetic pancreatic adenocarcinoma

    doi: 10.1007/s13402-026-01165-x

    Figure Lengend Snippet: Immune cell abundance and phenotype undergone significant alterations in diabetic PAAD. A Immune score and abundance of dendritic cells, B cells, and CD8 + T cells by xCell. B Expression level of immune-exhaustion markers in tumor samples of non-diabetic and diabetic PAAD patients. C Pearson correlation analyses between the expression of immune-exhaustion genes and immune cell markers. Pink and red circles indicate R value 0.3–0.8 and > 0.8, respectively. D Single cell type specificity of CD22 and TIGIT and their specific expression in bone marrow and lymph node immune cells from human single cell atlas

    Article Snippet: Harvested tumor paraffin samples were incubated with primary antibodies against CD8, TIGIT, CD19, CD22, Desmin, and CXCL12 (Cell Signaling Technology, Danvers, USA).

    Techniques: Expressing

    The distribution of immune-suppressive adaptive immune cells increased in diabetic PAAD. A The intratumoral distribution of CD22 + CD19 + B cells by multicolor immunofluorescence ( n = 10). Scale bar: 50 µm for upper part and 10 µm for lower part. B The intratumoral distribution of TIGIT + CD8 + T cells by multicolor immunofluorescence ( n = 10). Scale bar: 50 µm for upper part and 10 µm for lower part. C-D Body weight and blood glucose of BKS-WT and BKS-DB ( n = 3). E-F The phenotype estimation of CD8 + T cells and B cells by flow cytometry ( n = 3). All data were expressed as mean ± SD

    Journal: Cellular Oncology (Dordrecht, Netherlands)

    Article Title: CXCL12 derived from cancer-associated fibroblasts mediates dysfunctional intratumoral adaptive immunity in diabetic pancreatic adenocarcinoma

    doi: 10.1007/s13402-026-01165-x

    Figure Lengend Snippet: The distribution of immune-suppressive adaptive immune cells increased in diabetic PAAD. A The intratumoral distribution of CD22 + CD19 + B cells by multicolor immunofluorescence ( n = 10). Scale bar: 50 µm for upper part and 10 µm for lower part. B The intratumoral distribution of TIGIT + CD8 + T cells by multicolor immunofluorescence ( n = 10). Scale bar: 50 µm for upper part and 10 µm for lower part. C-D Body weight and blood glucose of BKS-WT and BKS-DB ( n = 3). E-F The phenotype estimation of CD8 + T cells and B cells by flow cytometry ( n = 3). All data were expressed as mean ± SD

    Article Snippet: Harvested tumor paraffin samples were incubated with primary antibodies against CD8, TIGIT, CD19, CD22, Desmin, and CXCL12 (Cell Signaling Technology, Danvers, USA).

    Techniques: Immunofluorescence, Flow Cytometry

    Overexpressed CXCL12 exacerbated in vivo adaptive immune migration and dysfunction in diabetic PAAD. A-C Schematic diagram of animal experiment and harvested subcutaneous tumors from different groups ( n = 6). D-E Estimation of intratumoral CD19 + B cells and CD8 + T cells distribution by IHC ( n = 6). Scale bar: 50 µm. F CD22 + percentage of CD19 + B cells by flow cytometry ( n = 5). G TIGIT expression of intratumoral CD8 + T cells in mPSC oe-NC , mPSC oe-CXCL12 , and mPSC oe-CXCL12 +plerixafor groups ( n = 5). All data were expressed as mean ± SD

    Journal: Cellular Oncology (Dordrecht, Netherlands)

    Article Title: CXCL12 derived from cancer-associated fibroblasts mediates dysfunctional intratumoral adaptive immunity in diabetic pancreatic adenocarcinoma

    doi: 10.1007/s13402-026-01165-x

    Figure Lengend Snippet: Overexpressed CXCL12 exacerbated in vivo adaptive immune migration and dysfunction in diabetic PAAD. A-C Schematic diagram of animal experiment and harvested subcutaneous tumors from different groups ( n = 6). D-E Estimation of intratumoral CD19 + B cells and CD8 + T cells distribution by IHC ( n = 6). Scale bar: 50 µm. F CD22 + percentage of CD19 + B cells by flow cytometry ( n = 5). G TIGIT expression of intratumoral CD8 + T cells in mPSC oe-NC , mPSC oe-CXCL12 , and mPSC oe-CXCL12 +plerixafor groups ( n = 5). All data were expressed as mean ± SD

    Article Snippet: Harvested tumor paraffin samples were incubated with primary antibodies against CD8, TIGIT, CD19, CD22, Desmin, and CXCL12 (Cell Signaling Technology, Danvers, USA).

    Techniques: In Vivo, Migration, Flow Cytometry, Expressing