Journal: bioRxiv

Article Title: Membrane localisation and checkpoint blockade enhance xenoantigen delivery to redirect pre-existing immunity against tumours

doi: 10.64898/2026.03.01.708859

Figure Lengend Snippet: A) Experimental timeline of the immunisation (i.e., vaccination) against OVA and subsequent tumour inoculation of the OVA-expressing B16F10 cell lines in mice. B) Titers of anti-OVA IgG per IgG subtypes in the plasma of the mice at d18. C) Percentage of OVA-specific CD8 + T cells against the immunogenic epitope OVA 257-264 (SIINFEKL) in the blood at d18 in pre-immunised mice (vax) or naïve mice (no vax) (n ≥ 3, mean ± SD, unpaired t-test). D, E) B16F10 melanoma cells, either wild-type (WT) or genetically modified to express high ( HI ) or low ( LO ) doses of membrane-bound OVA (B16mOVA) or soluble OVA (B16-OVA), were injected intradermally in C57BL/6 mice. Tumour growth (D) and associated survival (E) of the different OVA-expressing B16 cell lines in pre-immunised mice (n ≥ 5, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d10, d14 or d26 for tumour growth, log-rank tests for survival). F) Potential anti-tumour mechanisms engaged by soluble (left) or membrane-bound (right) xenoantigens when expressed by cancer cells.

Article Snippet: Samples were applied to the antigen coated plate and incubated at RT for 2 h. The plates were washed three times with PBST and HRP-conjugated antibodies were used to detect antigen-specific antibodies: anti-mouse IgG1 (#1070-05), anti-mouse IgG2a (#1080-05), anti-mouse IgG2b (#1090-05) and anti-mouse IgG3 (#1100-05) from Southern Biotech (Birmingham, AL, USA).

Techniques: Expressing, Clinical Proteomics, Genetically Modified, Membrane, Injection

Journal: bioRxiv

Article Title: Membrane localisation and checkpoint blockade enhance xenoantigen delivery to redirect pre-existing immunity against tumours

doi: 10.64898/2026.03.01.708859

Figure Lengend Snippet: A) Immunofluorescent staining of B16F10 WT melanoma with the TRP1-targeting TA99 antibody (scale bar = 100 μm). B) B16F10 WT tumour growth upon treatment with TA99 or IgG2a isotype control (n ≥ 4, mean ± SEM, Mann-Whitney test on d11). C) Design of FabTRP-OVA fusion protein and analysis of its production by SDS-PAGE (expected size = 92,3 kDa). D) Illustration of the FabTRP-OVA fusion protein approach for targeting the xenoantigen to the cancer cell membrane. E) Representative flow cytometry plot of FabTRP-OVA, OVA and no OVA (i.e., secondary antibody only) binding to the surface of B16F10 WT cells. F) B16F10 WT tumour growth when treated with FabTRP-OVA in pre-immunised or naïve mice (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). G) B16F10 WT tumour growth when treated with FabTRP-OVA in combination with anti-PD-1 checkpoint blocade therapy (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). H) Experimental treatment timeline of xenoantigen delivery (i.e., FabTRP-OVA, OVA or PBS (vehicle only)) and anti-PD-1 checkpoint blockade therapy in B16F10 WT in mice pre-immunised against OVA (Vax) or naïve (No vax). I, J) B16F10 WT tumour growth (I) and associated mouse survival (J) upon treatment with FabTRP-OVA, OVA or PBS in combination with anti-PD-1 checkpoint blockade therapy (n ≥ 5, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d16, log-rank tests for survival).

Article Snippet: Samples were applied to the antigen coated plate and incubated at RT for 2 h. The plates were washed three times with PBST and HRP-conjugated antibodies were used to detect antigen-specific antibodies: anti-mouse IgG1 (#1070-05), anti-mouse IgG2a (#1080-05), anti-mouse IgG2b (#1090-05) and anti-mouse IgG3 (#1100-05) from Southern Biotech (Birmingham, AL, USA).

Techniques: Staining, Control, MANN-WHITNEY, SDS Page, Membrane, Flow Cytometry, Binding Assay

Journal: bioRxiv

Article Title: Membrane localisation and checkpoint blockade enhance xenoantigen delivery to redirect pre-existing immunity against tumours

doi: 10.64898/2026.03.01.708859

Figure Lengend Snippet: A) Experimental timeline of the immunisation (i.e., vaccination) against varicella VZVO using Varivax or a combination of gE/CpG. B) IFΝγ quantification in the supernatant of gE restimulated (+) or non-restimulated (-) splenocytes, collected from mice immunized with Varivax, gE/CpG or PBS (i.e., naïve). Ionomycin+PMA was used as a positive control. C) Titers of anti-gE total IgG and per IgG subtypes in the plasma of the pre-immunised mice at d55 (before tumour implantation). D) Experimental treatment timeline of xenoantigen delivery (i.e., Varivax, gE or PBS (vehicle only)) and anti-PD-1 checkpoint blockade treatment in B16F10 WT in mice pre-immunised with Varivax against varicella VZVO . E, F) B16F10 WT tumour growth (E) and associated mouse survival (F) upon treatment with Varivax, gE or PBS in combination with anti-PD-1 checkpoint blockade (n ≥ 7, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d16, log-rank tests for survival).

Article Snippet: Samples were applied to the antigen coated plate and incubated at RT for 2 h. The plates were washed three times with PBST and HRP-conjugated antibodies were used to detect antigen-specific antibodies: anti-mouse IgG1 (#1070-05), anti-mouse IgG2a (#1080-05), anti-mouse IgG2b (#1090-05) and anti-mouse IgG3 (#1100-05) from Southern Biotech (Birmingham, AL, USA).

Techniques: Positive Control, Clinical Proteomics