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

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

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