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anti il 2rβ  (Bio X Cell)


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    Bio X Cell anti il 2rβ
    Anti Il 2rβ, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 94/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti il 2rβ/product/Bio X Cell
    Average 94 stars, based on 9 article reviews
    anti il 2rβ - by Bioz Stars, 2026-06
    94/100 stars

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    Bio X Cell invivomab anti mouse cd122 il 2rβ
    pH-responsive blocking and restoration of IL-2 receptor binding by UPS 5.3 (A) Schematic of the experimental design to assess the intrinsic interaction between UPS 5.3 micelles and proteins. (B) FPLC chromatograms showing individual proteins or UPS 5.3 /protein mixtures. (C) Molecular docking model of the DBA dimer (blue) with IL-2, highlighting predicted interaction sites. (D–F) Biolayer interferometry analysis of IL-2-Fc binding to IL-2Rα, <t>IL-2Rβ,</t> and IL-2Rγ, with and without UPS 5.3 NP encapsulation. (G) Schematic illustrating ex vivo assessment of IL-2-Fc binding to immune cells from various organs. (H) Quantification of IL-2-Fc binding to lymphocytes isolated from liver, lung, spleen, and tumor ( n = 5). Data are presented as mean ± SEM. See also and .
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    Proteintech il2rb
    RT-qPCR validation of the <t>IL2RB/IL2RG–EOMES–GZMA</t> cytotoxic/JAK axis in alopecia areata (AA). Relative mRNA levels of EOMES, GZMA, IL2RB, and IL2RG are significantly elevated in AA lesional scalp compared with healthy controls, whereas androgenetic alopecia (AGA) samples are comparable to controls, indicating that this cytotoxic/JAK module is transcriptionally active in AA but largely quiescent in AGA. Data are shown as mean ± SD. Statistical annotations: ** p < 0.01 vs. control; n.s., not significant (AGA vs. control).
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    Bio X Cell mouse cd122
    NK‐B Cells Represent a Subset of B‐Cell Progenitors. A) Monocle trajectories of wild‐type bone marrow lymphocytes from Tabula Muris database colored by cluster identity. Each dot represents a single cell. Cell orders are inferred from the expression of the most variable genes across all cells. The trajectory direction was determined by biological prior. Green dots indicated stem cells, pink dots indicated NK‐B cells and blue dots indicated B cells. B) Monocle trajectories of wild‐type bone marrow CD3 − NK1.1 + cells colored by cluster identity. Each dot represents a single cell. Cell orders are inferred from the expression of the most variable genes across all cells. The trajectory direction was determined by biological prior. Green dots indicated NK‐B cells and blue dots indicated CD27 − CD11b − immature NK cells. C) Representative percentage and D) flow cytometric plots of NK1.1 expression in pro‐B cells (CD43 + IgM − ), pre‐B cells (CD43 − IgM − ), immature B cells (B220 int IgM + ) and mature B cells (B220 + IgM + ) in the bone marrow of the indicated mice (n = 3). E) Schematic representation. CD3 − NK1.1 + CD19 + NK‐B cells from CD45.1 + mice bone marrow were sorted and transferred into CD45.2 + Rag1 −/− γc −/− mice and analyzed at 2 months. F) NK cells (CD3 − CD19 − NK1.1 + <t>CD122</t> + ), B cells (CD3 − CD19 + NK1.1 − ) and NK‐B cells (CD3 − CD19 + NK1.1 + ) existence was detected in recipient mice spleen and bone marrow. G) B cells development stage pro‐B cells (CD43 + IgM − ), pre‐B cells (CD43 − IgM − ), immature B cells (B220 int IgM + ) and mature B cells (B220 + IgM + ) existence was detected in recipient mice spleen and bone marrow (n = 3). H) Schemes depict four possible scenarios of NK‐B cell differentiation. Lymphocytes from indicated mice were isolated, stained with antibodies against CD3, CD19 and NK1.1 and analyzed by flow cytometry. CD3 − lymphocytes were gated out for analyzing NK1.1 versus CD19 I). Percentages of NK‐B cells (CD3 − CD19 + NK1.1 + ) J), NK cells (CD3 − CD19 − NK1.1 + ) K) and B cells (CD3 − CD19 + NK1.1 − ) L) were calculated (n = 3). Data represent the mean ± s.d. are representative of at least three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001. Unpaired Student's t ‐tests (two‐tailed) was used to calculate these values.
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    Bio X Cell anti cd122 il 15rβ antibody
    a , b The frequency of hepatic CD69 + T RM cells in WT APAP mice ( n = 3 per group per time point) ( a ) and in WT and Batf3-KO mice 24 h after APAP administration ( n = 3 per group) ( b ). c The frequency of Ki67 + cells in hepatic CD69 + KLRG1 − CD44 + CD8 + T RM cells in APAP mice. n = 4 per group. d The population of adoptively transferred OT-I T cells and of OT-I T RM cells in the liver of recipient mice after APAP administration. n = 3 per group. e The frequency of CD69 + T RM cells was assessed when APAP mice were pretreated with blocking antibodies against IL-12, IL-15 and IL-18. n = 4 per group. f The ALT level was assessed in APAP mice pretreated with IL-15 blocking antibodies <t>(α-CD122).</t> n = 3 per group per time point. g The frequency of IL-15Rα + cells in the hepatic DC1s and DC2s of APAP mice. n = 3 per group. h The frequency of T RM cells in hepatic CD8 + T cells when CD8 + T cells were cultured in the presence of IL-15. n = 4 per group. i The frequency of T RM cells among CD8 + T cells when hepatic CD8 + T cells were cocultured with LPS-stimulated hepatic DC1s of APAP mice in the presence of IL-15 blocking antibodies. n = 4 per group. Ordinary one-way ANOVA with Dunnett for posttest in a and e , unpaired two-tailed Student’s t -test in b – d and g – i and two-way ANOVA with Bonferroni for posttest in f were used to measure significance. The error bars indicate mean ± s.e.m. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001.
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    Image Search Results


    pH-responsive blocking and restoration of IL-2 receptor binding by UPS 5.3 (A) Schematic of the experimental design to assess the intrinsic interaction between UPS 5.3 micelles and proteins. (B) FPLC chromatograms showing individual proteins or UPS 5.3 /protein mixtures. (C) Molecular docking model of the DBA dimer (blue) with IL-2, highlighting predicted interaction sites. (D–F) Biolayer interferometry analysis of IL-2-Fc binding to IL-2Rα, IL-2Rβ, and IL-2Rγ, with and without UPS 5.3 NP encapsulation. (G) Schematic illustrating ex vivo assessment of IL-2-Fc binding to immune cells from various organs. (H) Quantification of IL-2-Fc binding to lymphocytes isolated from liver, lung, spleen, and tumor ( n = 5). Data are presented as mean ± SEM. See also and .

    Journal: Cell Reports Medicine

    Article Title: Targeting severe acidity for tumor-activatable Interleukin-2 therapy

    doi: 10.1016/j.xcrm.2025.102572

    Figure Lengend Snippet: pH-responsive blocking and restoration of IL-2 receptor binding by UPS 5.3 (A) Schematic of the experimental design to assess the intrinsic interaction between UPS 5.3 micelles and proteins. (B) FPLC chromatograms showing individual proteins or UPS 5.3 /protein mixtures. (C) Molecular docking model of the DBA dimer (blue) with IL-2, highlighting predicted interaction sites. (D–F) Biolayer interferometry analysis of IL-2-Fc binding to IL-2Rα, IL-2Rβ, and IL-2Rγ, with and without UPS 5.3 NP encapsulation. (G) Schematic illustrating ex vivo assessment of IL-2-Fc binding to immune cells from various organs. (H) Quantification of IL-2-Fc binding to lymphocytes isolated from liver, lung, spleen, and tumor ( n = 5). Data are presented as mean ± SEM. See also and .

    Article Snippet: InVivoMAb anti-mouse CD122 (IL-2Rβ) , BioXcell , Cat# BE0298 RRID: AB_2687820.

    Techniques: Blocking Assay, Binding Assay, Encapsulation, Ex Vivo, Isolation

    RT-qPCR validation of the IL2RB/IL2RG–EOMES–GZMA cytotoxic/JAK axis in alopecia areata (AA). Relative mRNA levels of EOMES, GZMA, IL2RB, and IL2RG are significantly elevated in AA lesional scalp compared with healthy controls, whereas androgenetic alopecia (AGA) samples are comparable to controls, indicating that this cytotoxic/JAK module is transcriptionally active in AA but largely quiescent in AGA. Data are shown as mean ± SD. Statistical annotations: ** p < 0.01 vs. control; n.s., not significant (AGA vs. control).

    Journal: Frontiers in Molecular Biosciences

    Article Title: JAK-centric explainable few-shot gene-expression diagnosis framework for alopecia via MultiPLIER priors and relation-style set-to-set comparison

    doi: 10.3389/fmolb.2025.1753206

    Figure Lengend Snippet: RT-qPCR validation of the IL2RB/IL2RG–EOMES–GZMA cytotoxic/JAK axis in alopecia areata (AA). Relative mRNA levels of EOMES, GZMA, IL2RB, and IL2RG are significantly elevated in AA lesional scalp compared with healthy controls, whereas androgenetic alopecia (AGA) samples are comparable to controls, indicating that this cytotoxic/JAK module is transcriptionally active in AA but largely quiescent in AGA. Data are shown as mean ± SD. Statistical annotations: ** p < 0.01 vs. control; n.s., not significant (AGA vs. control).

    Article Snippet: Equal amounts of protein were resolved by SDS–PAGE and transferred to PVDF membranes at 200 mA for 2 h. Membranes were blocked in 5% non-fat milk at room temperature for 2 h and incubated overnight at 4 ° C with primary antibodies against β -actin (1:4000; 20536-1-AP, Proteintech, China), EOMES (1:5000; 83945-5-RR, Proteintech, China), GZMA (1:500; 11288-1-AP, Proteintech, China), IL2RB (1:5000; 13602-1-AP, Proteintech, China), and IL2RG (1:500; 11409-1-AP, Proteintech, China).

    Techniques: Quantitative RT-PCR, Biomarker Discovery, Control

    GSEA plots for key genes. (a) EOMES. (b) GZMA. (c) IL2RB. (d) IL2RG.

    Journal: Frontiers in Molecular Biosciences

    Article Title: JAK-centric explainable few-shot gene-expression diagnosis framework for alopecia via MultiPLIER priors and relation-style set-to-set comparison

    doi: 10.3389/fmolb.2025.1753206

    Figure Lengend Snippet: GSEA plots for key genes. (a) EOMES. (b) GZMA. (c) IL2RB. (d) IL2RG.

    Article Snippet: Equal amounts of protein were resolved by SDS–PAGE and transferred to PVDF membranes at 200 mA for 2 h. Membranes were blocked in 5% non-fat milk at room temperature for 2 h and incubated overnight at 4 ° C with primary antibodies against β -actin (1:4000; 20536-1-AP, Proteintech, China), EOMES (1:5000; 83945-5-RR, Proteintech, China), GZMA (1:500; 11288-1-AP, Proteintech, China), IL2RB (1:5000; 13602-1-AP, Proteintech, China), and IL2RG (1:500; 11409-1-AP, Proteintech, China).

    Techniques:

    Western blot validation of the IL2RB/IL2RG–EOMES–GZMA cytotoxic/JAK axis at the protein level. Protein expression of EOMES, GZMA, IL2RB, and IL2RG is markedly upregulated in AA lesional scalp compared with healthy controls, concordant with the RT-qPCR results, whereas AGA-affected scalp shows no significant difference relative to controls. Representative immunoblots and densitometric quantification (normalized to β -actin) are shown. Data are presented as mean ± SD. Statistical annotations: ** p < 0.01 vs. control; n.s., not significant (AGA vs. control).

    Journal: Frontiers in Molecular Biosciences

    Article Title: JAK-centric explainable few-shot gene-expression diagnosis framework for alopecia via MultiPLIER priors and relation-style set-to-set comparison

    doi: 10.3389/fmolb.2025.1753206

    Figure Lengend Snippet: Western blot validation of the IL2RB/IL2RG–EOMES–GZMA cytotoxic/JAK axis at the protein level. Protein expression of EOMES, GZMA, IL2RB, and IL2RG is markedly upregulated in AA lesional scalp compared with healthy controls, concordant with the RT-qPCR results, whereas AGA-affected scalp shows no significant difference relative to controls. Representative immunoblots and densitometric quantification (normalized to β -actin) are shown. Data are presented as mean ± SD. Statistical annotations: ** p < 0.01 vs. control; n.s., not significant (AGA vs. control).

    Article Snippet: Equal amounts of protein were resolved by SDS–PAGE and transferred to PVDF membranes at 200 mA for 2 h. Membranes were blocked in 5% non-fat milk at room temperature for 2 h and incubated overnight at 4 ° C with primary antibodies against β -actin (1:4000; 20536-1-AP, Proteintech, China), EOMES (1:5000; 83945-5-RR, Proteintech, China), GZMA (1:500; 11288-1-AP, Proteintech, China), IL2RB (1:5000; 13602-1-AP, Proteintech, China), and IL2RG (1:500; 11409-1-AP, Proteintech, China).

    Techniques: Western Blot, Biomarker Discovery, Expressing, Quantitative RT-PCR, Control

    NK‐B Cells Represent a Subset of B‐Cell Progenitors. A) Monocle trajectories of wild‐type bone marrow lymphocytes from Tabula Muris database colored by cluster identity. Each dot represents a single cell. Cell orders are inferred from the expression of the most variable genes across all cells. The trajectory direction was determined by biological prior. Green dots indicated stem cells, pink dots indicated NK‐B cells and blue dots indicated B cells. B) Monocle trajectories of wild‐type bone marrow CD3 − NK1.1 + cells colored by cluster identity. Each dot represents a single cell. Cell orders are inferred from the expression of the most variable genes across all cells. The trajectory direction was determined by biological prior. Green dots indicated NK‐B cells and blue dots indicated CD27 − CD11b − immature NK cells. C) Representative percentage and D) flow cytometric plots of NK1.1 expression in pro‐B cells (CD43 + IgM − ), pre‐B cells (CD43 − IgM − ), immature B cells (B220 int IgM + ) and mature B cells (B220 + IgM + ) in the bone marrow of the indicated mice (n = 3). E) Schematic representation. CD3 − NK1.1 + CD19 + NK‐B cells from CD45.1 + mice bone marrow were sorted and transferred into CD45.2 + Rag1 −/− γc −/− mice and analyzed at 2 months. F) NK cells (CD3 − CD19 − NK1.1 + CD122 + ), B cells (CD3 − CD19 + NK1.1 − ) and NK‐B cells (CD3 − CD19 + NK1.1 + ) existence was detected in recipient mice spleen and bone marrow. G) B cells development stage pro‐B cells (CD43 + IgM − ), pre‐B cells (CD43 − IgM − ), immature B cells (B220 int IgM + ) and mature B cells (B220 + IgM + ) existence was detected in recipient mice spleen and bone marrow (n = 3). H) Schemes depict four possible scenarios of NK‐B cell differentiation. Lymphocytes from indicated mice were isolated, stained with antibodies against CD3, CD19 and NK1.1 and analyzed by flow cytometry. CD3 − lymphocytes were gated out for analyzing NK1.1 versus CD19 I). Percentages of NK‐B cells (CD3 − CD19 + NK1.1 + ) J), NK cells (CD3 − CD19 − NK1.1 + ) K) and B cells (CD3 − CD19 + NK1.1 − ) L) were calculated (n = 3). Data represent the mean ± s.d. are representative of at least three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001. Unpaired Student's t ‐tests (two‐tailed) was used to calculate these values.

    Journal: Advanced Science

    Article Title: A Microbiota‐ and IL‐15‐Dependent Innate‐Like B Cell Progenitor Expressing E4BP4

    doi: 10.1002/advs.202512444

    Figure Lengend Snippet: NK‐B Cells Represent a Subset of B‐Cell Progenitors. A) Monocle trajectories of wild‐type bone marrow lymphocytes from Tabula Muris database colored by cluster identity. Each dot represents a single cell. Cell orders are inferred from the expression of the most variable genes across all cells. The trajectory direction was determined by biological prior. Green dots indicated stem cells, pink dots indicated NK‐B cells and blue dots indicated B cells. B) Monocle trajectories of wild‐type bone marrow CD3 − NK1.1 + cells colored by cluster identity. Each dot represents a single cell. Cell orders are inferred from the expression of the most variable genes across all cells. The trajectory direction was determined by biological prior. Green dots indicated NK‐B cells and blue dots indicated CD27 − CD11b − immature NK cells. C) Representative percentage and D) flow cytometric plots of NK1.1 expression in pro‐B cells (CD43 + IgM − ), pre‐B cells (CD43 − IgM − ), immature B cells (B220 int IgM + ) and mature B cells (B220 + IgM + ) in the bone marrow of the indicated mice (n = 3). E) Schematic representation. CD3 − NK1.1 + CD19 + NK‐B cells from CD45.1 + mice bone marrow were sorted and transferred into CD45.2 + Rag1 −/− γc −/− mice and analyzed at 2 months. F) NK cells (CD3 − CD19 − NK1.1 + CD122 + ), B cells (CD3 − CD19 + NK1.1 − ) and NK‐B cells (CD3 − CD19 + NK1.1 + ) existence was detected in recipient mice spleen and bone marrow. G) B cells development stage pro‐B cells (CD43 + IgM − ), pre‐B cells (CD43 − IgM − ), immature B cells (B220 int IgM + ) and mature B cells (B220 + IgM + ) existence was detected in recipient mice spleen and bone marrow (n = 3). H) Schemes depict four possible scenarios of NK‐B cell differentiation. Lymphocytes from indicated mice were isolated, stained with antibodies against CD3, CD19 and NK1.1 and analyzed by flow cytometry. CD3 − lymphocytes were gated out for analyzing NK1.1 versus CD19 I). Percentages of NK‐B cells (CD3 − CD19 + NK1.1 + ) J), NK cells (CD3 − CD19 − NK1.1 + ) K) and B cells (CD3 − CD19 + NK1.1 − ) L) were calculated (n = 3). Data represent the mean ± s.d. are representative of at least three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001. Unpaired Student's t ‐tests (two‐tailed) was used to calculate these values.

    Article Snippet: [ ] Mouse CD122 (TM‐beta 1, #BE0298) and IgG2b isotype control (LTF‐2, #BE0090) were purchased from BioXcell.

    Techniques: Single Cell, Expressing, Cell Differentiation, Isolation, Staining, Flow Cytometry, Two Tailed Test

    IL‐15‐E4BP4 Axis and Microbiota Regulate NK‐B Cells Existence. A) Heat map illustrating the average transcript expression of the indicated genes (n = 3). The color key indicates the expression level. The expression levels of E4BP4, Eomes and T‐bet in B) NK cells (CD3 − CD19 − NK1.1 + ) and C) B cells (CD3 − CD19 + NK1.1 − ) from resting mice spleen and bone marrow. D) The expression levels of E4BP4, Eomes and T‐bet in NK‐B cells (CD3 − CD19 + NK1.1 + ) from resting mice spleen and bone marrow (n = 3). The expression levels of E4BP4 in NK‐B cells (CD3 − CD19 + NK1.1 + ) from E4BP4 reporter mice spleen and bone marrow stimulated with IL‐15 complex E,F) the absolute MFI (Zsgreen‐MFI) were quantified (n = 4). G) The expression levels of E4BP4 in NK cells (CD3 − CD19 − NK1.1 + ) and B cells (CD3 − CD19 + NK1.1 − ) from E4BP4 reporter mice spleen and bone marrow stimulated with IL‐15 complex. The absolute MFI (Zsgreen‐MFI) were quantified (n = 4). The expression levels of E4BP4 in CD122 + NK‐B cells and CD122 − NK‐B cells from E4BP4 reporter mice spleen and bone marrow stimulated with IL‐15 complex H,I) the absolute MFI (Zsgreen‐MFI) were quantified (n = 3). J) Absolute number of NK‐B (CD3 − CD19 + NK1.1 + ) (n = 5) and B (CD3 − CD19 + NK1.1 − ) (n = 4) cells in the spleen and bone marrow of the indicated mice. K) Absolute number of NK‐B (CD3 − CD19 + NK1.1 + ) cells in the spleen and bone marrow of the indicated mice (n = 5). Data represent the mean ± s.d. are representative of at least three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001. Unpaired Student's t ‐tests (two‐tailed) was used to calculate these values.

    Journal: Advanced Science

    Article Title: A Microbiota‐ and IL‐15‐Dependent Innate‐Like B Cell Progenitor Expressing E4BP4

    doi: 10.1002/advs.202512444

    Figure Lengend Snippet: IL‐15‐E4BP4 Axis and Microbiota Regulate NK‐B Cells Existence. A) Heat map illustrating the average transcript expression of the indicated genes (n = 3). The color key indicates the expression level. The expression levels of E4BP4, Eomes and T‐bet in B) NK cells (CD3 − CD19 − NK1.1 + ) and C) B cells (CD3 − CD19 + NK1.1 − ) from resting mice spleen and bone marrow. D) The expression levels of E4BP4, Eomes and T‐bet in NK‐B cells (CD3 − CD19 + NK1.1 + ) from resting mice spleen and bone marrow (n = 3). The expression levels of E4BP4 in NK‐B cells (CD3 − CD19 + NK1.1 + ) from E4BP4 reporter mice spleen and bone marrow stimulated with IL‐15 complex E,F) the absolute MFI (Zsgreen‐MFI) were quantified (n = 4). G) The expression levels of E4BP4 in NK cells (CD3 − CD19 − NK1.1 + ) and B cells (CD3 − CD19 + NK1.1 − ) from E4BP4 reporter mice spleen and bone marrow stimulated with IL‐15 complex. The absolute MFI (Zsgreen‐MFI) were quantified (n = 4). The expression levels of E4BP4 in CD122 + NK‐B cells and CD122 − NK‐B cells from E4BP4 reporter mice spleen and bone marrow stimulated with IL‐15 complex H,I) the absolute MFI (Zsgreen‐MFI) were quantified (n = 3). J) Absolute number of NK‐B (CD3 − CD19 + NK1.1 + ) (n = 5) and B (CD3 − CD19 + NK1.1 − ) (n = 4) cells in the spleen and bone marrow of the indicated mice. K) Absolute number of NK‐B (CD3 − CD19 + NK1.1 + ) cells in the spleen and bone marrow of the indicated mice (n = 5). Data represent the mean ± s.d. are representative of at least three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001. Unpaired Student's t ‐tests (two‐tailed) was used to calculate these values.

    Article Snippet: [ ] Mouse CD122 (TM‐beta 1, #BE0298) and IgG2b isotype control (LTF‐2, #BE0090) were purchased from BioXcell.

    Techniques: Expressing, Two Tailed Test

    a , b The frequency of hepatic CD69 + T RM cells in WT APAP mice ( n = 3 per group per time point) ( a ) and in WT and Batf3-KO mice 24 h after APAP administration ( n = 3 per group) ( b ). c The frequency of Ki67 + cells in hepatic CD69 + KLRG1 − CD44 + CD8 + T RM cells in APAP mice. n = 4 per group. d The population of adoptively transferred OT-I T cells and of OT-I T RM cells in the liver of recipient mice after APAP administration. n = 3 per group. e The frequency of CD69 + T RM cells was assessed when APAP mice were pretreated with blocking antibodies against IL-12, IL-15 and IL-18. n = 4 per group. f The ALT level was assessed in APAP mice pretreated with IL-15 blocking antibodies (α-CD122). n = 3 per group per time point. g The frequency of IL-15Rα + cells in the hepatic DC1s and DC2s of APAP mice. n = 3 per group. h The frequency of T RM cells in hepatic CD8 + T cells when CD8 + T cells were cultured in the presence of IL-15. n = 4 per group. i The frequency of T RM cells among CD8 + T cells when hepatic CD8 + T cells were cocultured with LPS-stimulated hepatic DC1s of APAP mice in the presence of IL-15 blocking antibodies. n = 4 per group. Ordinary one-way ANOVA with Dunnett for posttest in a and e , unpaired two-tailed Student’s t -test in b – d and g – i and two-way ANOVA with Bonferroni for posttest in f were used to measure significance. The error bars indicate mean ± s.e.m. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Experimental & Molecular Medicine

    Article Title: Discovery of intrahepatic CD103 + cDC1/CD8 + T RM protective immune axis against acetaminophen-induced acute liver injury

    doi: 10.1038/s12276-025-01565-3

    Figure Lengend Snippet: a , b The frequency of hepatic CD69 + T RM cells in WT APAP mice ( n = 3 per group per time point) ( a ) and in WT and Batf3-KO mice 24 h after APAP administration ( n = 3 per group) ( b ). c The frequency of Ki67 + cells in hepatic CD69 + KLRG1 − CD44 + CD8 + T RM cells in APAP mice. n = 4 per group. d The population of adoptively transferred OT-I T cells and of OT-I T RM cells in the liver of recipient mice after APAP administration. n = 3 per group. e The frequency of CD69 + T RM cells was assessed when APAP mice were pretreated with blocking antibodies against IL-12, IL-15 and IL-18. n = 4 per group. f The ALT level was assessed in APAP mice pretreated with IL-15 blocking antibodies (α-CD122). n = 3 per group per time point. g The frequency of IL-15Rα + cells in the hepatic DC1s and DC2s of APAP mice. n = 3 per group. h The frequency of T RM cells in hepatic CD8 + T cells when CD8 + T cells were cultured in the presence of IL-15. n = 4 per group. i The frequency of T RM cells among CD8 + T cells when hepatic CD8 + T cells were cocultured with LPS-stimulated hepatic DC1s of APAP mice in the presence of IL-15 blocking antibodies. n = 4 per group. Ordinary one-way ANOVA with Dunnett for posttest in a and e , unpaired two-tailed Student’s t -test in b – d and g – i and two-way ANOVA with Bonferroni for posttest in f were used to measure significance. The error bars indicate mean ± s.e.m. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: For IL-12, IL-15, IL-18 and CCL2 neutralizing, mice were i.p. injected with 200 μg per mouse of anti-IL-12 antibody (clone R1-5D9), anti-CD122 (IL-15Rβ) antibody (clone TM-Beta1), anti-IL-18 antibody (clone YIGIF74-1G7) and anti-CCL2 antibody (clone 2H5) (all from BioXCell).

    Techniques: Blocking Assay, Cell Culture, Two Tailed Test

    a Based on the public single-cell RNA sequencing dataset from liver tissues of healthy donors and patients with APAP-ALI ( GSE223581 ), the relative expression levels of IL-15 were assessed between APAP patients and healthy donors, and the correlation between IL-15 level and CD69 + T RM population among the CD8 + T cells was evaluated. b Using the same dataset, the frequency of CD14⁺ monocytes among total liver immune cells (left) and the populaton of FCGR3A⁺ inflammatory monocytes among the CD14 + monocytes in the liver (right) were assessed between healthy donors and patients with APAP-ALI. For inflammatory monocytes, the ratio of FCGR3A >0.1 was assessed in the CD14 >0.1 population of monocytes. c The mRNA levels of IL-15 / IL-15RA were assessed by quantitative real-time PCR in LPS-activated hepatic DC1s isolated from noncancerous healthy tissues of resected liver specimens obtained from patients with HCC and other liver diseases. n = 3 per group. d , e The frequency of human hepatic CD8 + T RM cells when hepatic CD8 + T cells were cocultured with LPS-treated hepatic DC1s ( d ), in the presence of IL-15 blocking antibodies (α-CD122) ( e ). f The human hepatic inflammatory monocytes were cocultured with human hepatic T RM cells at a different ratio, and the frequency of annexin V + monocytes was assessed. n = 4 per group. Unpaired two-tailed Student’s t -test in a and b , multiple unpaired t -test in c and ordinary one-way ANOVA with Dunnett for the posttest f were used to measure significance. The error bars indicate mean ± s.e.m. ns, not significant. * P < 0.05.

    Journal: Experimental & Molecular Medicine

    Article Title: Discovery of intrahepatic CD103 + cDC1/CD8 + T RM protective immune axis against acetaminophen-induced acute liver injury

    doi: 10.1038/s12276-025-01565-3

    Figure Lengend Snippet: a Based on the public single-cell RNA sequencing dataset from liver tissues of healthy donors and patients with APAP-ALI ( GSE223581 ), the relative expression levels of IL-15 were assessed between APAP patients and healthy donors, and the correlation between IL-15 level and CD69 + T RM population among the CD8 + T cells was evaluated. b Using the same dataset, the frequency of CD14⁺ monocytes among total liver immune cells (left) and the populaton of FCGR3A⁺ inflammatory monocytes among the CD14 + monocytes in the liver (right) were assessed between healthy donors and patients with APAP-ALI. For inflammatory monocytes, the ratio of FCGR3A >0.1 was assessed in the CD14 >0.1 population of monocytes. c The mRNA levels of IL-15 / IL-15RA were assessed by quantitative real-time PCR in LPS-activated hepatic DC1s isolated from noncancerous healthy tissues of resected liver specimens obtained from patients with HCC and other liver diseases. n = 3 per group. d , e The frequency of human hepatic CD8 + T RM cells when hepatic CD8 + T cells were cocultured with LPS-treated hepatic DC1s ( d ), in the presence of IL-15 blocking antibodies (α-CD122) ( e ). f The human hepatic inflammatory monocytes were cocultured with human hepatic T RM cells at a different ratio, and the frequency of annexin V + monocytes was assessed. n = 4 per group. Unpaired two-tailed Student’s t -test in a and b , multiple unpaired t -test in c and ordinary one-way ANOVA with Dunnett for the posttest f were used to measure significance. The error bars indicate mean ± s.e.m. ns, not significant. * P < 0.05.

    Article Snippet: For IL-12, IL-15, IL-18 and CCL2 neutralizing, mice were i.p. injected with 200 μg per mouse of anti-IL-12 antibody (clone R1-5D9), anti-CD122 (IL-15Rβ) antibody (clone TM-Beta1), anti-IL-18 antibody (clone YIGIF74-1G7) and anti-CCL2 antibody (clone 2H5) (all from BioXCell).

    Techniques: RNA Sequencing, Expressing, Real-time Polymerase Chain Reaction, Isolation, Blocking Assay, Two Tailed Test