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αil4 antibody  (Bio X Cell)


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    Bio X Cell αil4 antibody
    Biomaterial Injury Treatment Promotes Type-2 Immune Signature in CT26 Tumor Microenvironment. (A) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD4 + T cells (TH2) in VML-injured (untreated and ECM-treated) IL4-eGFP reporter (4Get) mice. CD4 + CD25 + (Tregs) were removed before TH2 gating (flow plot % are out of parent CD4 + CD25 - , which differs from bar graph depicting % out of all CD4 + ). (B) Differential gene expression and (C) normalized RNA transcript counts per million for type-2 cytokine genes from bulk RNAseq of CT26 tumor-infiltrating CD3 + T cells from uninjured and VML injured (untreated and ECM-treated) mice. (D) Intra-tumoral density of type-2 cytokine (IL4, IL5, IL13)-producing CT26 tumor-infiltrating CD4 + T cells from uninjured and VML injured (untreated and ECM-treated) mice following ex vivo cell stimulation. (E) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD11b + myeloid cells in VML injured (untreated and ECM-treated) 4Get mice. (F) Differential gene expression from bulk RNAseq of CT26 tumor-associated F480 + macrophages from untreated and ECM-treated VML injured mice. (G) Polarization of CT26 tumor-associated macrophages towards regenerative R1 (CD9 + CD301b + MHCII + ) phenotype in uninjured and VML injured (untreated and ECM-treated) mice. (Statistics) Bar graphs: mean±SD. For 2 groups, normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired, two-tailed student t-test ( A, E ). For >2 groups, data was analyzed using an ordinary one-way ANOVA with Tukey’s multiple comparisons test ( D, G ). Bulk RNAseq: Negative-binomial distribution using DeSeq2 with FDR correction for multiple testing (adjusted p-value thresholds indicated on plots) ( B, F ). No statistical analysis was performed on normalized transcript counts ( C ). NS: Not significant p>0.05, * p<0.05, ** p<0.01.
    αil4 Antibody, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 96/100, based on 176 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/αil4 antibody/product/Bio X Cell
    Average 96 stars, based on 176 article reviews
    αil4 antibody - by Bioz Stars, 2026-05
    96/100 stars

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    1) Product Images from "Tissue Injury and Biomaterial Treatment Modulate Tumor Growth and Response to Immunotherapy"

    Article Title: Tissue Injury and Biomaterial Treatment Modulate Tumor Growth and Response to Immunotherapy

    Journal: bioRxiv

    doi: 10.64898/2026.02.02.703323

    Biomaterial Injury Treatment Promotes Type-2 Immune Signature in CT26 Tumor Microenvironment. (A) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD4 + T cells (TH2) in VML-injured (untreated and ECM-treated) IL4-eGFP reporter (4Get) mice. CD4 + CD25 + (Tregs) were removed before TH2 gating (flow plot % are out of parent CD4 + CD25 - , which differs from bar graph depicting % out of all CD4 + ). (B) Differential gene expression and (C) normalized RNA transcript counts per million for type-2 cytokine genes from bulk RNAseq of CT26 tumor-infiltrating CD3 + T cells from uninjured and VML injured (untreated and ECM-treated) mice. (D) Intra-tumoral density of type-2 cytokine (IL4, IL5, IL13)-producing CT26 tumor-infiltrating CD4 + T cells from uninjured and VML injured (untreated and ECM-treated) mice following ex vivo cell stimulation. (E) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD11b + myeloid cells in VML injured (untreated and ECM-treated) 4Get mice. (F) Differential gene expression from bulk RNAseq of CT26 tumor-associated F480 + macrophages from untreated and ECM-treated VML injured mice. (G) Polarization of CT26 tumor-associated macrophages towards regenerative R1 (CD9 + CD301b + MHCII + ) phenotype in uninjured and VML injured (untreated and ECM-treated) mice. (Statistics) Bar graphs: mean±SD. For 2 groups, normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired, two-tailed student t-test ( A, E ). For >2 groups, data was analyzed using an ordinary one-way ANOVA with Tukey’s multiple comparisons test ( D, G ). Bulk RNAseq: Negative-binomial distribution using DeSeq2 with FDR correction for multiple testing (adjusted p-value thresholds indicated on plots) ( B, F ). No statistical analysis was performed on normalized transcript counts ( C ). NS: Not significant p>0.05, * p<0.05, ** p<0.01.
    Figure Legend Snippet: Biomaterial Injury Treatment Promotes Type-2 Immune Signature in CT26 Tumor Microenvironment. (A) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD4 + T cells (TH2) in VML-injured (untreated and ECM-treated) IL4-eGFP reporter (4Get) mice. CD4 + CD25 + (Tregs) were removed before TH2 gating (flow plot % are out of parent CD4 + CD25 - , which differs from bar graph depicting % out of all CD4 + ). (B) Differential gene expression and (C) normalized RNA transcript counts per million for type-2 cytokine genes from bulk RNAseq of CT26 tumor-infiltrating CD3 + T cells from uninjured and VML injured (untreated and ECM-treated) mice. (D) Intra-tumoral density of type-2 cytokine (IL4, IL5, IL13)-producing CT26 tumor-infiltrating CD4 + T cells from uninjured and VML injured (untreated and ECM-treated) mice following ex vivo cell stimulation. (E) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD11b + myeloid cells in VML injured (untreated and ECM-treated) 4Get mice. (F) Differential gene expression from bulk RNAseq of CT26 tumor-associated F480 + macrophages from untreated and ECM-treated VML injured mice. (G) Polarization of CT26 tumor-associated macrophages towards regenerative R1 (CD9 + CD301b + MHCII + ) phenotype in uninjured and VML injured (untreated and ECM-treated) mice. (Statistics) Bar graphs: mean±SD. For 2 groups, normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired, two-tailed student t-test ( A, E ). For >2 groups, data was analyzed using an ordinary one-way ANOVA with Tukey’s multiple comparisons test ( D, G ). Bulk RNAseq: Negative-binomial distribution using DeSeq2 with FDR correction for multiple testing (adjusted p-value thresholds indicated on plots) ( B, F ). No statistical analysis was performed on normalized transcript counts ( C ). NS: Not significant p>0.05, * p<0.05, ** p<0.01.

    Techniques Used: Gene Expression, RNA sequencing, Ex Vivo, Cell Stimulation, Two Tailed Test

    Biomaterial Injury Treatment-Induced Type-2 Immunity Also Develops in Tumor-Associated Tissues and Contributes to Delayed Tumor Growth. (A) Flow cytometric profiling of B and T lymphocytes, (b) Tregs (CD4 + FoxP3 + CD25 + ), and (C) CD8 + /Treg ratio in CT26 tumor-draining lymph nodes (tdLNs) of uninjured and VML-injured (untreated and ECM-treated) mice. (D) Frequency of IL4-eGFP + CD4 + T cells (TH2) in CT26 tdLNs of VML-injured (untreated and ECM-treated) 4Get mice. (E) Type-2 cytokine (IL4 and IL13) production by CD4 + T cells in CT26 tdLNs of uninjured and VML-injured (untreated and ECM-treated) mice following ex vivo cell stimulation. (F) Frequency of IL4-eGFP + SiglecF + eosinophils and CD4 + T cells in CT26 tumor-encapsulating adipose of VML-injured (untreated and ECM-treated) 4Get mice. (G) IL4 neutralization: CT26 tumor growth and survival curves of VML-injured (untreated and ECM-treated) mice treated with isotype (solid) or αIL4 antibody (1 mg/mouse initial dose followed by 0.5 mg/mouse maintenance) (dashed) (n=9-10). (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD. For 2 groups, normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired, two-tailed student t-test ( D, F ). For >2 groups, data was analyzed using an ordinary one-way ( A-C, E ) or two-way ( G - only D20 ) ANOVA with Tukey’s multiple comparisons test. Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( G ). NS: Not significant p>0.05, * p<0.05, ** p<0.01, *** p<0.001.
    Figure Legend Snippet: Biomaterial Injury Treatment-Induced Type-2 Immunity Also Develops in Tumor-Associated Tissues and Contributes to Delayed Tumor Growth. (A) Flow cytometric profiling of B and T lymphocytes, (b) Tregs (CD4 + FoxP3 + CD25 + ), and (C) CD8 + /Treg ratio in CT26 tumor-draining lymph nodes (tdLNs) of uninjured and VML-injured (untreated and ECM-treated) mice. (D) Frequency of IL4-eGFP + CD4 + T cells (TH2) in CT26 tdLNs of VML-injured (untreated and ECM-treated) 4Get mice. (E) Type-2 cytokine (IL4 and IL13) production by CD4 + T cells in CT26 tdLNs of uninjured and VML-injured (untreated and ECM-treated) mice following ex vivo cell stimulation. (F) Frequency of IL4-eGFP + SiglecF + eosinophils and CD4 + T cells in CT26 tumor-encapsulating adipose of VML-injured (untreated and ECM-treated) 4Get mice. (G) IL4 neutralization: CT26 tumor growth and survival curves of VML-injured (untreated and ECM-treated) mice treated with isotype (solid) or αIL4 antibody (1 mg/mouse initial dose followed by 0.5 mg/mouse maintenance) (dashed) (n=9-10). (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD. For 2 groups, normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired, two-tailed student t-test ( D, F ). For >2 groups, data was analyzed using an ordinary one-way ( A-C, E ) or two-way ( G - only D20 ) ANOVA with Tukey’s multiple comparisons test. Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( G ). NS: Not significant p>0.05, * p<0.05, ** p<0.01, *** p<0.001.

    Techniques Used: Ex Vivo, Cell Stimulation, Neutralization, Two Tailed Test



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    αil4 antibody  (Bio X Cell)
    96
    Bio X Cell αil4 antibody
    Biomaterial Injury Treatment Promotes Type-2 Immune Signature in CT26 Tumor Microenvironment. (A) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD4 + T cells (TH2) in VML-injured (untreated and ECM-treated) IL4-eGFP reporter (4Get) mice. CD4 + CD25 + (Tregs) were removed before TH2 gating (flow plot % are out of parent CD4 + CD25 - , which differs from bar graph depicting % out of all CD4 + ). (B) Differential gene expression and (C) normalized RNA transcript counts per million for type-2 cytokine genes from bulk RNAseq of CT26 tumor-infiltrating CD3 + T cells from uninjured and VML injured (untreated and ECM-treated) mice. (D) Intra-tumoral density of type-2 cytokine (IL4, IL5, IL13)-producing CT26 tumor-infiltrating CD4 + T cells from uninjured and VML injured (untreated and ECM-treated) mice following ex vivo cell stimulation. (E) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD11b + myeloid cells in VML injured (untreated and ECM-treated) 4Get mice. (F) Differential gene expression from bulk RNAseq of CT26 tumor-associated F480 + macrophages from untreated and ECM-treated VML injured mice. (G) Polarization of CT26 tumor-associated macrophages towards regenerative R1 (CD9 + CD301b + MHCII + ) phenotype in uninjured and VML injured (untreated and ECM-treated) mice. (Statistics) Bar graphs: mean±SD. For 2 groups, normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired, two-tailed student t-test ( A, E ). For >2 groups, data was analyzed using an ordinary one-way ANOVA with Tukey’s multiple comparisons test ( D, G ). Bulk RNAseq: Negative-binomial distribution using DeSeq2 with FDR correction for multiple testing (adjusted p-value thresholds indicated on plots) ( B, F ). No statistical analysis was performed on normalized transcript counts ( C ). NS: Not significant p>0.05, * p<0.05, ** p<0.01.
    αil4 Antibody, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/αil4 antibody/product/Bio X Cell
    Average 96 stars, based on 1 article reviews
    αil4 antibody - by Bioz Stars, 2026-05
    96/100 stars
    		  Buy from Supplier

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    Biomaterial Injury Treatment Promotes Type-2 Immune Signature in CT26 Tumor Microenvironment. (A) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD4 + T cells (TH2) in VML-injured (untreated and ECM-treated) IL4-eGFP reporter (4Get) mice. CD4 + CD25 + (Tregs) were removed before TH2 gating (flow plot % are out of parent CD4 + CD25 - , which differs from bar graph depicting % out of all CD4 + ). (B) Differential gene expression and (C) normalized RNA transcript counts per million for type-2 cytokine genes from bulk RNAseq of CT26 tumor-infiltrating CD3 + T cells from uninjured and VML injured (untreated and ECM-treated) mice. (D) Intra-tumoral density of type-2 cytokine (IL4, IL5, IL13)-producing CT26 tumor-infiltrating CD4 + T cells from uninjured and VML injured (untreated and ECM-treated) mice following ex vivo cell stimulation. (E) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD11b + myeloid cells in VML injured (untreated and ECM-treated) 4Get mice. (F) Differential gene expression from bulk RNAseq of CT26 tumor-associated F480 + macrophages from untreated and ECM-treated VML injured mice. (G) Polarization of CT26 tumor-associated macrophages towards regenerative R1 (CD9 + CD301b + MHCII + ) phenotype in uninjured and VML injured (untreated and ECM-treated) mice. (Statistics) Bar graphs: mean±SD. For 2 groups, normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired, two-tailed student t-test ( A, E ). For >2 groups, data was analyzed using an ordinary one-way ANOVA with Tukey’s multiple comparisons test ( D, G ). Bulk RNAseq: Negative-binomial distribution using DeSeq2 with FDR correction for multiple testing (adjusted p-value thresholds indicated on plots) ( B, F ). No statistical analysis was performed on normalized transcript counts ( C ). NS: Not significant p>0.05, * p<0.05, ** p<0.01.

    Journal: bioRxiv

    Article Title: Tissue Injury and Biomaterial Treatment Modulate Tumor Growth and Response to Immunotherapy

    doi: 10.64898/2026.02.02.703323

    Figure Lengend Snippet: Biomaterial Injury Treatment Promotes Type-2 Immune Signature in CT26 Tumor Microenvironment. (A) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD4 + T cells (TH2) in VML-injured (untreated and ECM-treated) IL4-eGFP reporter (4Get) mice. CD4 + CD25 + (Tregs) were removed before TH2 gating (flow plot % are out of parent CD4 + CD25 - , which differs from bar graph depicting % out of all CD4 + ). (B) Differential gene expression and (C) normalized RNA transcript counts per million for type-2 cytokine genes from bulk RNAseq of CT26 tumor-infiltrating CD3 + T cells from uninjured and VML injured (untreated and ECM-treated) mice. (D) Intra-tumoral density of type-2 cytokine (IL4, IL5, IL13)-producing CT26 tumor-infiltrating CD4 + T cells from uninjured and VML injured (untreated and ECM-treated) mice following ex vivo cell stimulation. (E) Frequency of CT26 tumor-infiltrating IL4-eGFP + CD11b + myeloid cells in VML injured (untreated and ECM-treated) 4Get mice. (F) Differential gene expression from bulk RNAseq of CT26 tumor-associated F480 + macrophages from untreated and ECM-treated VML injured mice. (G) Polarization of CT26 tumor-associated macrophages towards regenerative R1 (CD9 + CD301b + MHCII + ) phenotype in uninjured and VML injured (untreated and ECM-treated) mice. (Statistics) Bar graphs: mean±SD. For 2 groups, normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired, two-tailed student t-test ( A, E ). For >2 groups, data was analyzed using an ordinary one-way ANOVA with Tukey’s multiple comparisons test ( D, G ). Bulk RNAseq: Negative-binomial distribution using DeSeq2 with FDR correction for multiple testing (adjusted p-value thresholds indicated on plots) ( B, F ). No statistical analysis was performed on normalized transcript counts ( C ). NS: Not significant p>0.05, * p<0.05, ** p<0.01.

    Article Snippet: IL4 was neutralized using αIL4 antibody (clone 11B11, BioXCell BE0045) delivered via IP injection prepared in sterile dilution buffer ( InVivo Pure pH 7.0, BioXCell IP0070).

    Techniques: Gene Expression, RNA sequencing, Ex Vivo, Cell Stimulation, Two Tailed Test

    Biomaterial Injury Treatment-Induced Type-2 Immunity Also Develops in Tumor-Associated Tissues and Contributes to Delayed Tumor Growth. (A) Flow cytometric profiling of B and T lymphocytes, (b) Tregs (CD4 + FoxP3 + CD25 + ), and (C) CD8 + /Treg ratio in CT26 tumor-draining lymph nodes (tdLNs) of uninjured and VML-injured (untreated and ECM-treated) mice. (D) Frequency of IL4-eGFP + CD4 + T cells (TH2) in CT26 tdLNs of VML-injured (untreated and ECM-treated) 4Get mice. (E) Type-2 cytokine (IL4 and IL13) production by CD4 + T cells in CT26 tdLNs of uninjured and VML-injured (untreated and ECM-treated) mice following ex vivo cell stimulation. (F) Frequency of IL4-eGFP + SiglecF + eosinophils and CD4 + T cells in CT26 tumor-encapsulating adipose of VML-injured (untreated and ECM-treated) 4Get mice. (G) IL4 neutralization: CT26 tumor growth and survival curves of VML-injured (untreated and ECM-treated) mice treated with isotype (solid) or αIL4 antibody (1 mg/mouse initial dose followed by 0.5 mg/mouse maintenance) (dashed) (n=9-10). (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD. For 2 groups, normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired, two-tailed student t-test ( D, F ). For >2 groups, data was analyzed using an ordinary one-way ( A-C, E ) or two-way ( G - only D20 ) ANOVA with Tukey’s multiple comparisons test. Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( G ). NS: Not significant p>0.05, * p<0.05, ** p<0.01, *** p<0.001.

    Journal: bioRxiv

    Article Title: Tissue Injury and Biomaterial Treatment Modulate Tumor Growth and Response to Immunotherapy

    doi: 10.64898/2026.02.02.703323

    Figure Lengend Snippet: Biomaterial Injury Treatment-Induced Type-2 Immunity Also Develops in Tumor-Associated Tissues and Contributes to Delayed Tumor Growth. (A) Flow cytometric profiling of B and T lymphocytes, (b) Tregs (CD4 + FoxP3 + CD25 + ), and (C) CD8 + /Treg ratio in CT26 tumor-draining lymph nodes (tdLNs) of uninjured and VML-injured (untreated and ECM-treated) mice. (D) Frequency of IL4-eGFP + CD4 + T cells (TH2) in CT26 tdLNs of VML-injured (untreated and ECM-treated) 4Get mice. (E) Type-2 cytokine (IL4 and IL13) production by CD4 + T cells in CT26 tdLNs of uninjured and VML-injured (untreated and ECM-treated) mice following ex vivo cell stimulation. (F) Frequency of IL4-eGFP + SiglecF + eosinophils and CD4 + T cells in CT26 tumor-encapsulating adipose of VML-injured (untreated and ECM-treated) 4Get mice. (G) IL4 neutralization: CT26 tumor growth and survival curves of VML-injured (untreated and ECM-treated) mice treated with isotype (solid) or αIL4 antibody (1 mg/mouse initial dose followed by 0.5 mg/mouse maintenance) (dashed) (n=9-10). (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD. For 2 groups, normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired, two-tailed student t-test ( D, F ). For >2 groups, data was analyzed using an ordinary one-way ( A-C, E ) or two-way ( G - only D20 ) ANOVA with Tukey’s multiple comparisons test. Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( G ). NS: Not significant p>0.05, * p<0.05, ** p<0.01, *** p<0.001.

    Article Snippet: IL4 was neutralized using αIL4 antibody (clone 11B11, BioXCell BE0045) delivered via IP injection prepared in sterile dilution buffer ( InVivo Pure pH 7.0, BioXCell IP0070).

    Techniques: Ex Vivo, Cell Stimulation, Neutralization, Two Tailed Test