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primary rabbit antibodies against mouse apoa1  (Proteintech)


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    Proteintech primary rabbit antibodies against mouse apoa1
    Primary Rabbit Antibodies Against Mouse Apoa1, supplied by Proteintech, used in various techniques. Bioz Stars score: 92/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary rabbit antibodies against mouse apoa1/product/Proteintech
    Average 92 stars, based on 16 article reviews
    primary rabbit antibodies against mouse apoa1 - by Bioz Stars, 2026-05
    92/100 stars

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    Primary Antibodies Against Embmhc Mouse Monoclonal, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    A Proportions of CD3+, <t>CD8</t> +, and CD4 + T cells by flow cytometry in control and aCD40 treated Brpkp110 tumors on day 13 post treatment ( n = 10). B FoxP3 + CD4+ regulatory T cells on day 7 post-treatment ( n = 7). C Proportions of Granzyme B + T cells in subpopulations by flow cytometry in control and aCD40 treated Brpkp110 tumors on day 7 post implantation ( n = 10). D Images of immunofluorescent staining for CD8 (red) and nuclei (blue) and CD8 staining quantification in untreated (control) and aCD40 treated Brpkp110 tumors on day 7 post treatment ( n = 4–6). E Quantification of CD8 immunofluorescent staining in outer, middle, and inner thirds of control and aCD40 treated tumors on day 7 post treatment ( n = 5–6). F After 7 days of treatment with aCD40, Brpkp110 tumors were minced and cultured ex vivo. Supernatant was collected and pooled for each treatment group after 48 h and cytokines were measured ( n = 2, with 3 tumors pooled per group). G T cell activation and proliferation markers measured by flow cytometry in CD4+ and CD8 + T cell populations of control and aCD40 treated Brpkp110 TDLN on day 7 post-treatment ( n = 10). H Growth curves of control and aCD40 treated Brpkp110 tumors implanted into WT hosts with or without T cell depletions ( n = 17–20). I Tumor growth curve of aCD40 (treatment on Day 8) +/− FTY720 (treatment started on Day 7) treated Brpkp110 tumors ( n = 14–16). Data: ( A – C , D (right), E – G ) median, ( H , I ) mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.
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    A Proportions of CD3+, <t>CD8</t> +, and CD4 + T cells by flow cytometry in control and aCD40 treated Brpkp110 tumors on day 13 post treatment ( n = 10). B FoxP3 + CD4+ regulatory T cells on day 7 post-treatment ( n = 7). C Proportions of Granzyme B + T cells in subpopulations by flow cytometry in control and aCD40 treated Brpkp110 tumors on day 7 post implantation ( n = 10). D Images of immunofluorescent staining for CD8 (red) and nuclei (blue) and CD8 staining quantification in untreated (control) and aCD40 treated Brpkp110 tumors on day 7 post treatment ( n = 4–6). E Quantification of CD8 immunofluorescent staining in outer, middle, and inner thirds of control and aCD40 treated tumors on day 7 post treatment ( n = 5–6). F After 7 days of treatment with aCD40, Brpkp110 tumors were minced and cultured ex vivo. Supernatant was collected and pooled for each treatment group after 48 h and cytokines were measured ( n = 2, with 3 tumors pooled per group). G T cell activation and proliferation markers measured by flow cytometry in CD4+ and CD8 + T cell populations of control and aCD40 treated Brpkp110 TDLN on day 7 post-treatment ( n = 10). H Growth curves of control and aCD40 treated Brpkp110 tumors implanted into WT hosts with or without T cell depletions ( n = 17–20). I Tumor growth curve of aCD40 (treatment on Day 8) +/− FTY720 (treatment started on Day 7) treated Brpkp110 tumors ( n = 14–16). Data: ( A – C , D (right), E – G ) median, ( H , I ) mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.
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    Cell Signaling Technology Inc rabbit anti mouse anti eea 1 primary antibody
    A Proportions of CD3+, <t>CD8</t> +, and CD4 + T cells by flow cytometry in control and aCD40 treated Brpkp110 tumors on day 13 post treatment ( n = 10). B FoxP3 + CD4+ regulatory T cells on day 7 post-treatment ( n = 7). C Proportions of Granzyme B + T cells in subpopulations by flow cytometry in control and aCD40 treated Brpkp110 tumors on day 7 post implantation ( n = 10). D Images of immunofluorescent staining for CD8 (red) and nuclei (blue) and CD8 staining quantification in untreated (control) and aCD40 treated Brpkp110 tumors on day 7 post treatment ( n = 4–6). E Quantification of CD8 immunofluorescent staining in outer, middle, and inner thirds of control and aCD40 treated tumors on day 7 post treatment ( n = 5–6). F After 7 days of treatment with aCD40, Brpkp110 tumors were minced and cultured ex vivo. Supernatant was collected and pooled for each treatment group after 48 h and cytokines were measured ( n = 2, with 3 tumors pooled per group). G T cell activation and proliferation markers measured by flow cytometry in CD4+ and CD8 + T cell populations of control and aCD40 treated Brpkp110 TDLN on day 7 post-treatment ( n = 10). H Growth curves of control and aCD40 treated Brpkp110 tumors implanted into WT hosts with or without T cell depletions ( n = 17–20). I Tumor growth curve of aCD40 (treatment on Day 8) +/− FTY720 (treatment started on Day 7) treated Brpkp110 tumors ( n = 14–16). Data: ( A – C , D (right), E – G ) median, ( H , I ) mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.
    Rabbit Anti Mouse Anti Eea 1 Primary Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    A) RNASeq (left) and RT-qPCR (right) reveal upregulation of the NF-κB signaling target genes nfkbiaa and nfkbiab in osteoblasts sorted from bglap:GFP fish heterozygous for the wnt10a mutation relative to their wild-type siblings at 1 dpa. nE (qPCR biological replicates) = 3, nA = 10 per replicate. ΔΔCt values are normalized to the mean of the wildtype at 1 dpa. Error bars, Mean ± SEM. Two tailed Student’s t-test. B) Osteoblast dedifferentiation, as measured by bglap downregulation in segment -1 revealed by HCR in situ hybridization, is inhibited in fish treated with the Wnt inhibitor IWR-1, while IP injection of the NF-κB inhibitor Bay-11 slightly but significantly enhances dedifferentiation. Treatment with both inhibitors yields results similar to those of Bay-11 alone. nE = 3 (except for 2 for IWR-1), nA = 18 total per group (12 for IWR-1), nR = 33 (DMSO), 24 (IWR-1), 37 (Bay-11), 33 (both). C) Overexpression of wnt10a using hs:wnt10a fish is sufficient to cause downregulation of bglapl detected by HCR in situ hybridization in non-injured fins, relative to heat-shocked wild-type fish. HCR signals were quantified in a bony segment (“B”) that is located at the same proximal-distal position as “segment -1” in amputated fins. nE = 2, nA = 12 total per group, nR = 22 total per group. Dashed line, joints. Scale bar, 100 µm. D) Immunofluorescence on cryosections of hs:wnt10a transgenic hearts reveals increased embryonic myosin heavy chain (embMHC) expression in Myl7+ cardiomyocytes at the wound border at 7 days post injury (dpi). Plots show the ventricular area covered by anti-embMHC staining relative to the 150 µm wound border zone area occupied by Myl7+ myocardium. nE = 2, nA = 13 wild-type, 11 hs:wnt10a . Scale bar, 100 µm. (B, C, D) Error bars, mean ± 95% CI. Two tailed Student’s t-test.

    Journal: bioRxiv

    Article Title: Wnt/β-catenin signaling promotes zebrafish osteoblast dedifferentiation by wnt10a -mediated inhibition of NF-κB

    doi: 10.64898/2025.12.29.696582

    Figure Lengend Snippet: A) RNASeq (left) and RT-qPCR (right) reveal upregulation of the NF-κB signaling target genes nfkbiaa and nfkbiab in osteoblasts sorted from bglap:GFP fish heterozygous for the wnt10a mutation relative to their wild-type siblings at 1 dpa. nE (qPCR biological replicates) = 3, nA = 10 per replicate. ΔΔCt values are normalized to the mean of the wildtype at 1 dpa. Error bars, Mean ± SEM. Two tailed Student’s t-test. B) Osteoblast dedifferentiation, as measured by bglap downregulation in segment -1 revealed by HCR in situ hybridization, is inhibited in fish treated with the Wnt inhibitor IWR-1, while IP injection of the NF-κB inhibitor Bay-11 slightly but significantly enhances dedifferentiation. Treatment with both inhibitors yields results similar to those of Bay-11 alone. nE = 3 (except for 2 for IWR-1), nA = 18 total per group (12 for IWR-1), nR = 33 (DMSO), 24 (IWR-1), 37 (Bay-11), 33 (both). C) Overexpression of wnt10a using hs:wnt10a fish is sufficient to cause downregulation of bglapl detected by HCR in situ hybridization in non-injured fins, relative to heat-shocked wild-type fish. HCR signals were quantified in a bony segment (“B”) that is located at the same proximal-distal position as “segment -1” in amputated fins. nE = 2, nA = 12 total per group, nR = 22 total per group. Dashed line, joints. Scale bar, 100 µm. D) Immunofluorescence on cryosections of hs:wnt10a transgenic hearts reveals increased embryonic myosin heavy chain (embMHC) expression in Myl7+ cardiomyocytes at the wound border at 7 days post injury (dpi). Plots show the ventricular area covered by anti-embMHC staining relative to the 150 µm wound border zone area occupied by Myl7+ myocardium. nE = 2, nA = 13 wild-type, 11 hs:wnt10a . Scale bar, 100 µm. (B, C, D) Error bars, mean ± 95% CI. Two tailed Student’s t-test.

    Article Snippet: Primary antibodies against embMHC Mouse monoclonal (MYH7 DSHB, N2.261, RRID:AB_531790), and Myl7 Rabbit polyclonal (GeneTex, GTX128346, RRID:AB_2885759) were diluted in PEMTx/normal goad serum and applied overnight at 4 °C.

    Techniques: Quantitative RT-PCR, Mutagenesis, Two Tailed Test, In Situ Hybridization, Injection, Over Expression, Immunofluorescence, Transgenic Assay, Expressing, Staining

    (A) Schematic of a sagittal view of the zebrafish brain highlighting the proximate location of the diencephalic posterior tubercular nucleus (PTN) and innervation of the Mauthner cells (M-cell). (B) Confocal projections of PCNA expression in a representative communal, dominant, and subordinate Tg( dat :egfp) zebrafish. Merged channel also shows DAPI nuclear staining in blue. Arrowheads point to PCNA expressing PTN somata. Scale bar = 20 μm. (C) Summary graph of the fraction of PTN neurons that express PCNA. Symbols represent individual samples; bars represent averages, error bars represent SEM. Dashed lines show pairwise comparison connecting each dominant to its subordinate counterpart. (Com n=6, Dom n= 8, Sub n= 8; One-way ANOVA, P=0.0029 , One-way ANOVA, Tukey’s Multiple Comparison post-test).

    Journal: bioRxiv

    Article Title: Cellular mechanisms underlying social regulation of the posterior tubercular nucleus in zebrafish ( Danio rerio )

    doi: 10.64898/2026.01.27.701991

    Figure Lengend Snippet: (A) Schematic of a sagittal view of the zebrafish brain highlighting the proximate location of the diencephalic posterior tubercular nucleus (PTN) and innervation of the Mauthner cells (M-cell). (B) Confocal projections of PCNA expression in a representative communal, dominant, and subordinate Tg( dat :egfp) zebrafish. Merged channel also shows DAPI nuclear staining in blue. Arrowheads point to PCNA expressing PTN somata. Scale bar = 20 μm. (C) Summary graph of the fraction of PTN neurons that express PCNA. Symbols represent individual samples; bars represent averages, error bars represent SEM. Dashed lines show pairwise comparison connecting each dominant to its subordinate counterpart. (Com n=6, Dom n= 8, Sub n= 8; One-way ANOVA, P=0.0029 , One-way ANOVA, Tukey’s Multiple Comparison post-test).

    Article Snippet: Another series of PBS washes (3-4 times for 5 minutes each) was performed, and slices were stained with a rabbit polyclonal anti-PCNA primary antibody (Cell Signaling, 2586t) at a concentration of 1:500.

    Techniques: Expressing, Staining, Comparison

    (A) PC1 and PC2 are the first and the second principal components excluding social isolates. (B) Eigenvalues of the principal components excluding social isolates showing the percentage of variation explained by each component. Line plot illustrates the cumulative explained variance. (C) PC1 and PC2 are the first and the second Principal components excluding PCNA as a component. (D) Eigenvalues of the principal components excluding PNCA as a component showing the percentage of variation explained by each component. Line plot illustrates the cumulative explained variance. In A and C, points represent individual samples (n= 6 per social condition), different colors and symbols represent different groups. Ellipses represent 68% confidence intervals of core regions. Loading vectors represent original variables, the directions of arrows represent correlation between original variable and principal components, lengths represent association of original data to principal components. In B and D components are listed in descending order (highest to the lowest).

    Journal: bioRxiv

    Article Title: Cellular mechanisms underlying social regulation of the posterior tubercular nucleus in zebrafish ( Danio rerio )

    doi: 10.64898/2026.01.27.701991

    Figure Lengend Snippet: (A) PC1 and PC2 are the first and the second principal components excluding social isolates. (B) Eigenvalues of the principal components excluding social isolates showing the percentage of variation explained by each component. Line plot illustrates the cumulative explained variance. (C) PC1 and PC2 are the first and the second Principal components excluding PCNA as a component. (D) Eigenvalues of the principal components excluding PNCA as a component showing the percentage of variation explained by each component. Line plot illustrates the cumulative explained variance. In A and C, points represent individual samples (n= 6 per social condition), different colors and symbols represent different groups. Ellipses represent 68% confidence intervals of core regions. Loading vectors represent original variables, the directions of arrows represent correlation between original variable and principal components, lengths represent association of original data to principal components. In B and D components are listed in descending order (highest to the lowest).

    Article Snippet: Another series of PBS washes (3-4 times for 5 minutes each) was performed, and slices were stained with a rabbit polyclonal anti-PCNA primary antibody (Cell Signaling, 2586t) at a concentration of 1:500.

    Techniques:

    A Proportions of CD3+, CD8 +, and CD4 + T cells by flow cytometry in control and aCD40 treated Brpkp110 tumors on day 13 post treatment ( n = 10). B FoxP3 + CD4+ regulatory T cells on day 7 post-treatment ( n = 7). C Proportions of Granzyme B + T cells in subpopulations by flow cytometry in control and aCD40 treated Brpkp110 tumors on day 7 post implantation ( n = 10). D Images of immunofluorescent staining for CD8 (red) and nuclei (blue) and CD8 staining quantification in untreated (control) and aCD40 treated Brpkp110 tumors on day 7 post treatment ( n = 4–6). E Quantification of CD8 immunofluorescent staining in outer, middle, and inner thirds of control and aCD40 treated tumors on day 7 post treatment ( n = 5–6). F After 7 days of treatment with aCD40, Brpkp110 tumors were minced and cultured ex vivo. Supernatant was collected and pooled for each treatment group after 48 h and cytokines were measured ( n = 2, with 3 tumors pooled per group). G T cell activation and proliferation markers measured by flow cytometry in CD4+ and CD8 + T cell populations of control and aCD40 treated Brpkp110 TDLN on day 7 post-treatment ( n = 10). H Growth curves of control and aCD40 treated Brpkp110 tumors implanted into WT hosts with or without T cell depletions ( n = 17–20). I Tumor growth curve of aCD40 (treatment on Day 8) +/− FTY720 (treatment started on Day 7) treated Brpkp110 tumors ( n = 14–16). Data: ( A – C , D (right), E – G ) median, ( H , I ) mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Journal: NPJ Breast Cancer

    Article Title: Agonistic CD40 elicits CD8+ T-cell-dependent primary responses and CD4+ T-cell-dependent long-term immunity in breast cancer

    doi: 10.1038/s41523-025-00889-7

    Figure Lengend Snippet: A Proportions of CD3+, CD8 +, and CD4 + T cells by flow cytometry in control and aCD40 treated Brpkp110 tumors on day 13 post treatment ( n = 10). B FoxP3 + CD4+ regulatory T cells on day 7 post-treatment ( n = 7). C Proportions of Granzyme B + T cells in subpopulations by flow cytometry in control and aCD40 treated Brpkp110 tumors on day 7 post implantation ( n = 10). D Images of immunofluorescent staining for CD8 (red) and nuclei (blue) and CD8 staining quantification in untreated (control) and aCD40 treated Brpkp110 tumors on day 7 post treatment ( n = 4–6). E Quantification of CD8 immunofluorescent staining in outer, middle, and inner thirds of control and aCD40 treated tumors on day 7 post treatment ( n = 5–6). F After 7 days of treatment with aCD40, Brpkp110 tumors were minced and cultured ex vivo. Supernatant was collected and pooled for each treatment group after 48 h and cytokines were measured ( n = 2, with 3 tumors pooled per group). G T cell activation and proliferation markers measured by flow cytometry in CD4+ and CD8 + T cell populations of control and aCD40 treated Brpkp110 TDLN on day 7 post-treatment ( n = 10). H Growth curves of control and aCD40 treated Brpkp110 tumors implanted into WT hosts with or without T cell depletions ( n = 17–20). I Tumor growth curve of aCD40 (treatment on Day 8) +/− FTY720 (treatment started on Day 7) treated Brpkp110 tumors ( n = 14–16). Data: ( A – C , D (right), E – G ) median, ( H , I ) mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Article Snippet: Tissue sections were blocked with 5% donkey serum diluted in PBS with 0.3% Triton X-100 and stained with rabbit anti-mouse primary CD8 (clone: D4W2Z, Cell Signaling Technology 98941, 1:100) followed by donkey anti-rabbit Alexa Fluor 594 (Thermo Scientific A-21207, 1:250) secondary antibody.

    Techniques: Flow Cytometry, Control, Staining, Cell Culture, Ex Vivo, Activation Assay

    A Tumor growth curves (left) and tumor volume changes compared to pretreatment on day 26 post implantation (right) of Brpkp110 tumors. Indicated treatments initiated on day 7 post implantation ( n = 18–20). B Tumor growth curves (left) and tumor volume changes compared to pretreatment on day 26 post implantation (right) of E0771 tumors. Indicated treatments initiated on day 8 post implantation ( n = 12–15). C Tumor growth curves (left) and tumor volume changes compared to pretreatment on day 31 post implantation (right) of AT3 tumors. Indicated treatments initiated on day 9 post implantation ( n = 14). D Tumor growth curves (left) and tumor volume changes compared to pretreatment on day 34 post implantation (right) of EpH4 1424 tumors. Indicated treatments initiated on day 5 post implantation ( n = 14–16). E Brpkp110 tumor growth curves (left) and volume changes compared to pretreatment (right) on day 27 post implantation in control and aCD40+ICB treated hosts with and without CD8 + T cell depletions. Indicated treatments initiated on day 7 post implantation ( n = 12–15). F Brpkp110 tumor growth curves (left) and volume changes compared to pretreatment (right) on day 25 post implantation in control and aCD40+ICB treated hosts with and without CD4 + T cell depletions. Indicated treatments initiated on day 8 post implantation ( n = 14–18). G Brpkp110 tumor growth curves (left) and volume changes compared to pretreatment (right) on day 27 post implantation in control and aCD40+ICB treated hosts with and without CD4+ and CD8 + T cell depletions. Indicated treatments initiated on day 7 post implantation ( n = 12–18). H Tumor growth curves (left) and volume changes compared to pretreatment (right) on day 26 post Brpkp110 tumor implantation into WT and BATF3 KO hosts. Indicated treatments initiated on day 7 post implantation ( n = 14–18). Data: ( A – H left) mean ± SEM, ( A – H right) each column represents individual tumor. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Journal: NPJ Breast Cancer

    Article Title: Agonistic CD40 elicits CD8+ T-cell-dependent primary responses and CD4+ T-cell-dependent long-term immunity in breast cancer

    doi: 10.1038/s41523-025-00889-7

    Figure Lengend Snippet: A Tumor growth curves (left) and tumor volume changes compared to pretreatment on day 26 post implantation (right) of Brpkp110 tumors. Indicated treatments initiated on day 7 post implantation ( n = 18–20). B Tumor growth curves (left) and tumor volume changes compared to pretreatment on day 26 post implantation (right) of E0771 tumors. Indicated treatments initiated on day 8 post implantation ( n = 12–15). C Tumor growth curves (left) and tumor volume changes compared to pretreatment on day 31 post implantation (right) of AT3 tumors. Indicated treatments initiated on day 9 post implantation ( n = 14). D Tumor growth curves (left) and tumor volume changes compared to pretreatment on day 34 post implantation (right) of EpH4 1424 tumors. Indicated treatments initiated on day 5 post implantation ( n = 14–16). E Brpkp110 tumor growth curves (left) and volume changes compared to pretreatment (right) on day 27 post implantation in control and aCD40+ICB treated hosts with and without CD8 + T cell depletions. Indicated treatments initiated on day 7 post implantation ( n = 12–15). F Brpkp110 tumor growth curves (left) and volume changes compared to pretreatment (right) on day 25 post implantation in control and aCD40+ICB treated hosts with and without CD4 + T cell depletions. Indicated treatments initiated on day 8 post implantation ( n = 14–18). G Brpkp110 tumor growth curves (left) and volume changes compared to pretreatment (right) on day 27 post implantation in control and aCD40+ICB treated hosts with and without CD4+ and CD8 + T cell depletions. Indicated treatments initiated on day 7 post implantation ( n = 12–18). H Tumor growth curves (left) and volume changes compared to pretreatment (right) on day 26 post Brpkp110 tumor implantation into WT and BATF3 KO hosts. Indicated treatments initiated on day 7 post implantation ( n = 14–18). Data: ( A – H left) mean ± SEM, ( A – H right) each column represents individual tumor. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Article Snippet: Tissue sections were blocked with 5% donkey serum diluted in PBS with 0.3% Triton X-100 and stained with rabbit anti-mouse primary CD8 (clone: D4W2Z, Cell Signaling Technology 98941, 1:100) followed by donkey anti-rabbit Alexa Fluor 594 (Thermo Scientific A-21207, 1:250) secondary antibody.

    Techniques: Control, Tumor Implantation

    A Proportions of circulating effector memory (CD44 + CD62L-), central memory (CD44 + CD62L+), and naïve (CD44-CD62L-) CD4+ (left) and CD8+ (right) in blood, 3 months post treatment induced tumor clearance ( n = 5–6, data representative of 2 experiments with similar results). B Secondary Brpkp110 tumor rechallenge of naïve and previously Brpkp110 tumor-bearing mice cured after aCD40 + ICB, at least 2 months post primary tumor clearance ( n = 12–14, data representative of 3 experiments with similar results). C Control and rechallenge tumor growth in T cell sufficient ( n = 6–12) and T cell depleted hosts ( n = 12–14, data representative of 2 experiments with similar results). D Brpkp110 tumor growth curves in intra-tumoral (IT) vehicle (control) and IT aCD40 treated hosts. aCD40 administered tumors denoted as aCD40 IT and contralateral untreated tumors denoted as CD40 IT Distant ( n = 9–12, data representative of 2 experiments with similar results). E Brpkp110 tumor growth curves in intra-tumoral (IT) vehicle (control) and IT or intraperitoneal (IP) aCD40 or ICB received hosts ( n = 4–9, data representative of 2 experiments with similar results). Data: ( A ) median, ( C – E ) mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Journal: NPJ Breast Cancer

    Article Title: Agonistic CD40 elicits CD8+ T-cell-dependent primary responses and CD4+ T-cell-dependent long-term immunity in breast cancer

    doi: 10.1038/s41523-025-00889-7

    Figure Lengend Snippet: A Proportions of circulating effector memory (CD44 + CD62L-), central memory (CD44 + CD62L+), and naïve (CD44-CD62L-) CD4+ (left) and CD8+ (right) in blood, 3 months post treatment induced tumor clearance ( n = 5–6, data representative of 2 experiments with similar results). B Secondary Brpkp110 tumor rechallenge of naïve and previously Brpkp110 tumor-bearing mice cured after aCD40 + ICB, at least 2 months post primary tumor clearance ( n = 12–14, data representative of 3 experiments with similar results). C Control and rechallenge tumor growth in T cell sufficient ( n = 6–12) and T cell depleted hosts ( n = 12–14, data representative of 2 experiments with similar results). D Brpkp110 tumor growth curves in intra-tumoral (IT) vehicle (control) and IT aCD40 treated hosts. aCD40 administered tumors denoted as aCD40 IT and contralateral untreated tumors denoted as CD40 IT Distant ( n = 9–12, data representative of 2 experiments with similar results). E Brpkp110 tumor growth curves in intra-tumoral (IT) vehicle (control) and IT or intraperitoneal (IP) aCD40 or ICB received hosts ( n = 4–9, data representative of 2 experiments with similar results). Data: ( A ) median, ( C – E ) mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Article Snippet: Tissue sections were blocked with 5% donkey serum diluted in PBS with 0.3% Triton X-100 and stained with rabbit anti-mouse primary CD8 (clone: D4W2Z, Cell Signaling Technology 98941, 1:100) followed by donkey anti-rabbit Alexa Fluor 594 (Thermo Scientific A-21207, 1:250) secondary antibody.

    Techniques: Control