Journal: Journal of Neuroinflammation

Article Title: CD22 modulation alleviates amyloid β-induced neuroinflammation

doi: 10.1186/s12974-025-03361-2

Figure Lengend Snippet: CD22 promotes neuroinflammation via microglia. A Schematic diagram of sCD22 i.c.v. injection into wildtype C57BL/6 mice. B Volcano plot of sCD22-treated mouse cortex after 3 days treatment. N = 3. C-D Gene ontology analysis of sCD22-treated mice (3 days treatment) in KEGG pathway ( C ) and Biological function ( D ). E Volcano plot of sCD22-treated mouse cortex after 7 days treatment. N = 4. F Gene ontology analysis of sCD22-treated mice (7 days treatment) in Biological function. G GSEA showing enrichment of IL6/JAK/STAT3, TNFα Signaling via NFκB, and Cholesterol Homeostasis of mouse cortex after sCD22 7 days treatment relative to PBS group. H Representative image and quantitation showing the effect of sCD22 on IbaI and GFAP expression in mouse cortex. IbaI: Student t -test, ** P < 0.01; GFAP: ns: not significant. N = 6. I Schematic diagram of MDMi differentiation and sCD22 treatment. J Principal component analysis showing sCD22 treated MDMi versus control MDMi. N = 4. K Volcano plot of sCD22-treated MDMi. L Gene ontology analysis of sCD22-treated MDMi in Biological function. M Gene ontology analysis of sCD22-treated MDMi in KEGG

Article Snippet: All other materials included RPMI-1640 (Gibco, A10491-01), Dulbecco’s modified Eagle’s medium (DMEM) (Gibco, 11995-040), FBS (Gibco, A5256701), Pen/strep (Gibco, 15140-122), IL-34 (Sino Biological, 10948-H08S), GM-CSF (Sino Biological, 10015-HNAH), Geltrex (Gibco, A14133-02), human CD22 ECD (CD22 FL) (Sino Biological, 11958-H08H), human CD22 a.a. 176–687 (CD22 δ1) (Sino Biological, 11958-H08H1), mouse CD22 ECD (Sino Biological, 51177-M08H), Tanzisertib (Selleckchem, S8490), Perifosine (Selleckchem, S1037), Ravoxertinib (Selleckchem, S7554), SB856553 (Selleckchem, S7215).

Techniques: Injection, Quantitation Assay, Expressing, Control

Journal: Journal of Neuroinflammation

Article Title: CD22 modulation alleviates amyloid β-induced neuroinflammation

doi: 10.1186/s12974-025-03361-2

Figure Lengend Snippet: sCD22 promotes microglial neuroinflammation via MAPK-signaling pathway and in a sialic acid-dependent manner. A Immunostaining with anti-IbaI antibody to examine microglia activation after sCD22 treatment in MDMi. Student t -test, **** P < 0.0001, ns: not significant. N = 26–27, from 3 independent experiments. B-D Effect of sCD22 on viability of MDMi ( B ), HMC-3 ( C ) and BV-2 cells ( D ). E Representative and quantitation of western blot examining ERK1/2 and p38 phosphorylation in sCD22-treated MDMi. p38: One-way ANOVA, F = 16.01, P = 0.001, Tukey post hoc test ** P < 0.01; ERK1/2: One-way ANOVA, F = 7.38, P = 0.0108, Tukey post hoc test * P < 0.05. F Effect of ERK1/2 inhibitor (Ravoxertinib) and p38 inhibitor (SB856553) on sCD22-mediated TNFα, IL-6 & CCL3 release. TNFα: One-way ANOVA, F = 16.09, Tukey post hoc test **** P < 0.0001; IL-6: One-way ANOVA, F = 4.917, Tukey post hoc test * P < 0.05, ** P < 0.01; CCL3: One-way ANOVA, F = 6.672, Tukey post hoc test ** P < 0.01. N = 4–5. G Effect of pan JNK inhibitor (Tanzisertib) and Akt inhibitor (Perifosine) on sCD22-mediated CCL3 release. H Schematic diagram of sCD22 with complete extracellular domain (CD22-FL) and with D1-truncated (CD22-δ1). I Full length and D1-truncated sCD22 effect on TNFα, IL-6 & CCL3 release in MDMi. TNFα: One-way ANOVA, F = 7.847, Tukey post hoc test * P < 0.05, ** P < 0.01; IL-6: One-way ANOVA, F = 4.375, Tukey post hoc test * P < 0.05; CCL3: One-way ANOVA, F = 3.669, Tukey post hoc test * P < 0.05. ns: not significant. N = 5–6. J Effect of CHO-derived sCD22 on CCL3 release in MDMi. Student t -test, P = 0.83. N = 2. K Effect of HEK293-derived sCD22 and CHO-derived sCD22 on CCL3 release in THP-1. Two-way ANOVA, source of sCD22: F (1,4) = 124, P = 0.0007; CCL3 release: F (1,4) = 87.57, P = 0.0007. Tukey post hoc test, i < 0.001. ns: not significant. N = 2. All data are presented as mean ± SEM

Article Snippet: All other materials included RPMI-1640 (Gibco, A10491-01), Dulbecco’s modified Eagle’s medium (DMEM) (Gibco, 11995-040), FBS (Gibco, A5256701), Pen/strep (Gibco, 15140-122), IL-34 (Sino Biological, 10948-H08S), GM-CSF (Sino Biological, 10015-HNAH), Geltrex (Gibco, A14133-02), human CD22 ECD (CD22 FL) (Sino Biological, 11958-H08H), human CD22 a.a. 176–687 (CD22 δ1) (Sino Biological, 11958-H08H1), mouse CD22 ECD (Sino Biological, 51177-M08H), Tanzisertib (Selleckchem, S8490), Perifosine (Selleckchem, S1037), Ravoxertinib (Selleckchem, S7554), SB856553 (Selleckchem, S7215).

Techniques: Immunostaining, Activation Assay, Quantitation Assay, Western Blot, Derivative Assay

Journal: Journal of Neuroinflammation

Article Title: CD22 modulation alleviates amyloid β-induced neuroinflammation

doi: 10.1186/s12974-025-03361-2

Figure Lengend Snippet: CD22 modulation by suciraslimab alleviates Aβ-induced neuroinflammation in human CD22 transgenic mice. A Schematic diagram of Aβ-induced neuroinflammation model in human CD22 transgenic mice. B Effect of suciraslimab on Aβ-injected model mice in Y-maze test. Alternation: One-way ANOVA, F = 4.724, P = 0.0196. Tukey post hoc test, * P < 0.05. Number of arm entry: One-way ANOVA, F = 0.07, P = 0.93. N = 8–9. C Volcano plot of suciraslimab-treated mouse cortex. N = 3. D Gene ontology analysis of suciraslimab-treated mouse cortex in Biological function. E Gene ontology analysis of suciraslimab-treated mouse cortex in molecular function. F Effect of suciraslimab on chemokine release in mouse brain of model mice. Student t -test, P value as stated in the figure. N = 3. All data are presented as mean ± SEM

Article Snippet: All other materials included RPMI-1640 (Gibco, A10491-01), Dulbecco’s modified Eagle’s medium (DMEM) (Gibco, 11995-040), FBS (Gibco, A5256701), Pen/strep (Gibco, 15140-122), IL-34 (Sino Biological, 10948-H08S), GM-CSF (Sino Biological, 10015-HNAH), Geltrex (Gibco, A14133-02), human CD22 ECD (CD22 FL) (Sino Biological, 11958-H08H), human CD22 a.a. 176–687 (CD22 δ1) (Sino Biological, 11958-H08H1), mouse CD22 ECD (Sino Biological, 51177-M08H), Tanzisertib (Selleckchem, S8490), Perifosine (Selleckchem, S1037), Ravoxertinib (Selleckchem, S7554), SB856553 (Selleckchem, S7215).

Techniques: Transgenic Assay, Injection

Journal: Journal of Neuroinflammation

Article Title: CD22 modulation alleviates amyloid β-induced neuroinflammation

doi: 10.1186/s12974-025-03361-2

Figure Lengend Snippet: Suciraslimab suppresses Aβ-induced inflammation in microglia and human PBMC. A Effect of CD22 overexpression on Aβ-induced NFκB signaling in HEK293. Two-way ANOVA: CD22 expression, F (1,20) = 62.97, i < 0.0001; Aβ treatment, F (4,20) = 16.83, P < 0.0001. Tukey post hoc test, **** P < 0.0001. N = 3. B Effect of suciraslimab on Aβ-induced IL-1β release in MDMi. One-way ANOVA, F = 7.767, P = 0.004. Tuley post hoc test, * P < 0.05, ** P < 0.01. N = 6–7. C Immunofluorescent staining and quantitation of NLRP3 and ASC after Aβ and suciraslimab treatment in MDMi. NLRP3: One-way ANOVA, F = 10.09, P < 0.0001, Tukey post hoc test * P < 0.05, *** P < 0.001; ASC, One-way ANOVA, F = 19.10, P < 0.0001, Tukey post hoc test **** P < 0.0001. N = 6–15. D Effect of suciraslimab on Aβ-induced IL-1β release in human PBMC. One-way ANOVA, F = 6.833, P = 0.0052. Tukey post hoc test, ** P < 0.01, ns = not significant. N = 8. E Effect of suciraslimab on IFNγ + LPS-induced IL-23 and IL-12 release in human PBMC. IL-23: One-way ANOVA, F = 26.93, P = 0.0002. Tukey post hoc test, ** P < 0.01, *** P < 0.001; IL-12: One-way ANOVA, F = 10.21, P = 0.0008. Tukey post hoc test, * P < 0.05, *** P < 0.001. N = 4–8. F Effect of suciraslimab on TLR4 surface expression on monocyte upon IFNγ and LPS activation. Two-tailed paired Student’s t test, P = 0.0293, t = 3.322, df = 4. N = 5 G Effect of suciraslimab on α4 integrin surface expression on T cell of human PBMC. One-way ANOVA, F = 0.7059, P = 0.5131. N = 5. H Effect of suciraslimab on α4 integrin surface expression on B cell of human PBMC. One-way ANOVA, F = 66.02, P < 0.0001. Tukey’s post hoc test, * P < 0.05, **** P < 0.0001. N = 4–5. I Effect of suciraslimab on α4 integrin surface expression on T cell-depleted human PBMC. One-way ANOVA, F = 16.91, P = 0.0009. Tukey’s post hoc test, ** P < 0.01. N = 4. J Effect of suciraslimab on α4 integrin surface expression on monocyte-depleted human PBMC. One-way ANOVA, F = 8.565, P = 0.0083. Tukey’s post hoc test, IgG1 vs. αCD22 Ab, P = 0.1748. N = 4. All data are presented as mean ± SEM

Article Snippet: All other materials included RPMI-1640 (Gibco, A10491-01), Dulbecco’s modified Eagle’s medium (DMEM) (Gibco, 11995-040), FBS (Gibco, A5256701), Pen/strep (Gibco, 15140-122), IL-34 (Sino Biological, 10948-H08S), GM-CSF (Sino Biological, 10015-HNAH), Geltrex (Gibco, A14133-02), human CD22 ECD (CD22 FL) (Sino Biological, 11958-H08H), human CD22 a.a. 176–687 (CD22 δ1) (Sino Biological, 11958-H08H1), mouse CD22 ECD (Sino Biological, 51177-M08H), Tanzisertib (Selleckchem, S8490), Perifosine (Selleckchem, S1037), Ravoxertinib (Selleckchem, S7554), SB856553 (Selleckchem, S7215).

Techniques: Over Expression, Expressing, Staining, Quantitation Assay, Activation Assay, Two Tailed Test

Journal: Journal of Neuroinflammation

Article Title: CD22 modulation alleviates amyloid β-induced neuroinflammation

doi: 10.1186/s12974-025-03361-2

Figure Lengend Snippet: Suciraslimab promotes Aβ phagocytosis. A BLI analysis of mouse CD22-Aβ interaction. Association: 600s; Dissociation: 600s. B BLI analysis of human CD22-Aβ interaction. Association: 600s; Dissociation: 600s. C Immunofluorescent staining and quantitation of FITC-Aβ on HEK293 and HEK293-hCD22 cells. Student t -test, ** P < 0.01. N = 20–21, from 3 independent experiments. D Representative image and quantitation of Proximity-ligation assay of CD22-Aβ complex in HMC-3. Student’s t -test, **** P < 0.0001. N = 41, from 3 independent experiments. E Structural alignment of mouse CD22 and human CD22. The structures of both mouse and human CD22 extracellular domain were generated with Alphafold2. Pairwise structural alignment score (TM-score) higher than 0.5 assumes generally proteins aligned of the same fold. F Surface CD22 expression in HMC-3 after suciraslimab treatment. One-way ANOVA, F = 2.892, P = 0.0139. Tukey post hoc test, * P < 0.05. N = 76–83. G Surface suciraslimab binding on HMC-3. One-way ANOVA, F = 125, P < 0.0001. Tukey post hoc test, ** P = 0.002. N = 3. H Effect of suciraslimab on FITC-Aβ phagocytosis in HMC-3. One-way ANOVA, F = 43.92, P < 0.0001. Tukey post hoc test, * P = 0.046, ** P = 0.0018, **** P < 0.0001. N = 3. I Effect of suciraslimab on FITC-Aβ phagocytosis in PMA-differentiated MO3.13. Two-tailed Student’s t test, P = 0.0477, t = 2.482, df = 6

Article Snippet: All other materials included RPMI-1640 (Gibco, A10491-01), Dulbecco’s modified Eagle’s medium (DMEM) (Gibco, 11995-040), FBS (Gibco, A5256701), Pen/strep (Gibco, 15140-122), IL-34 (Sino Biological, 10948-H08S), GM-CSF (Sino Biological, 10015-HNAH), Geltrex (Gibco, A14133-02), human CD22 ECD (CD22 FL) (Sino Biological, 11958-H08H), human CD22 a.a. 176–687 (CD22 δ1) (Sino Biological, 11958-H08H1), mouse CD22 ECD (Sino Biological, 51177-M08H), Tanzisertib (Selleckchem, S8490), Perifosine (Selleckchem, S1037), Ravoxertinib (Selleckchem, S7554), SB856553 (Selleckchem, S7215).

Techniques: Staining, Quantitation Assay, Proximity Ligation Assay, Generated, Expressing, Binding Assay, Two Tailed Test

Journal: Molecular cell

Article Title: An Atlas of Human Glycosylation Pathways Enables Display of the Human Glycome by Gene Engineered Cells

doi: 10.1016/j.molcel.2019.05.017

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Biotinylated lectins (Vector Laboratories, Burlingame, CA) were incubated at different concentrations for 1 h, followed by washing and incubation with Streptavidin-Alexa Fluor488 (Invitrogen) for 1 h. Recombinant human Siglec Fc-chimera (R&D systems, Minneapolis, MN) were precomplexed with Alexa Fluor647 goat anti-human IgG antibody (Life Technologies) for 1 h followed by incubation with cells for 1 hr.

Techniques: Recombinant, Plasmid Preparation, Construct, Software