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mouse il 36β  (R&D Systems)


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    R&D Systems mouse il 36β
    <t>IL-36β</t> KO mice exhibit altered responses to HSV-1 skin infection. a Wild type (WT; n = 5 ♀ and 13 ♂) and IL-36β KO mice ( n = 7 ♀ and 12 ♂) were infected with HSV-1 on the flank and skin regions along HSV-1 infected dermatomes collected 6 days post-infection. Viral DNA loads were determined by QPCR. Data are pooled from three independent experiments and shown as means ( ± SD). * p < 0.05 (One-Way ANOVA). b , c Viral ICP4 protein levels were examined by Western blotting ( b ) and quantified using ImageJ software ( c ). GAPDH was used as loading control. Data are representative of three independent experiments and shown as means (±SD) in c (WT: n = 2 female and 4 male; IL-36β KO mice: n = 3 female and 3 male). * p < 0.05 (one-way ANOVA). d Wild type and IL - 36β KO mice were infected with HSV-1 ( n = 3 per group) on the flank and skin RNA isolated 6 days post-infection. Heat-map of genes differentially expressed in the two strains is shown. e Pathway associations of genes identified as differentially expressed in d . f Expression of Oas1 , Eif2ak2, Isg15, Ifitm3, Ifitm2, and Ifit3 mRNAs were examined in wild type and IL-36β KO HSV-1 infected skin ( a ). The mRNAs were normalized against GAPDH and are shown as relative expression compared to female wild-type mice (means ± SD). * p < 0.05; ** p < 0.005 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file
    Mouse Il 36β, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse il 36β/product/R&D Systems
    Average 93 stars, based on 4 article reviews
    mouse il 36β - by Bioz Stars, 2026-05
    93/100 stars

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    1) Product Images from "IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners"

    Article Title: IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners

    Journal: Nature Communications

    doi: 10.1038/s41467-019-12318-y

    IL-36β KO mice exhibit altered responses to HSV-1 skin infection. a Wild type (WT; n = 5 ♀ and 13 ♂) and IL-36β KO mice ( n = 7 ♀ and 12 ♂) were infected with HSV-1 on the flank and skin regions along HSV-1 infected dermatomes collected 6 days post-infection. Viral DNA loads were determined by QPCR. Data are pooled from three independent experiments and shown as means ( ± SD). * p < 0.05 (One-Way ANOVA). b , c Viral ICP4 protein levels were examined by Western blotting ( b ) and quantified using ImageJ software ( c ). GAPDH was used as loading control. Data are representative of three independent experiments and shown as means (±SD) in c (WT: n = 2 female and 4 male; IL-36β KO mice: n = 3 female and 3 male). * p < 0.05 (one-way ANOVA). d Wild type and IL - 36β KO mice were infected with HSV-1 ( n = 3 per group) on the flank and skin RNA isolated 6 days post-infection. Heat-map of genes differentially expressed in the two strains is shown. e Pathway associations of genes identified as differentially expressed in d . f Expression of Oas1 , Eif2ak2, Isg15, Ifitm3, Ifitm2, and Ifit3 mRNAs were examined in wild type and IL-36β KO HSV-1 infected skin ( a ). The mRNAs were normalized against GAPDH and are shown as relative expression compared to female wild-type mice (means ± SD). * p < 0.05; ** p < 0.005 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file
    Figure Legend Snippet: IL-36β KO mice exhibit altered responses to HSV-1 skin infection. a Wild type (WT; n = 5 ♀ and 13 ♂) and IL-36β KO mice ( n = 7 ♀ and 12 ♂) were infected with HSV-1 on the flank and skin regions along HSV-1 infected dermatomes collected 6 days post-infection. Viral DNA loads were determined by QPCR. Data are pooled from three independent experiments and shown as means ( ± SD). * p < 0.05 (One-Way ANOVA). b , c Viral ICP4 protein levels were examined by Western blotting ( b ) and quantified using ImageJ software ( c ). GAPDH was used as loading control. Data are representative of three independent experiments and shown as means (±SD) in c (WT: n = 2 female and 4 male; IL-36β KO mice: n = 3 female and 3 male). * p < 0.05 (one-way ANOVA). d Wild type and IL - 36β KO mice were infected with HSV-1 ( n = 3 per group) on the flank and skin RNA isolated 6 days post-infection. Heat-map of genes differentially expressed in the two strains is shown. e Pathway associations of genes identified as differentially expressed in d . f Expression of Oas1 , Eif2ak2, Isg15, Ifitm3, Ifitm2, and Ifit3 mRNAs were examined in wild type and IL-36β KO HSV-1 infected skin ( a ). The mRNAs were normalized against GAPDH and are shown as relative expression compared to female wild-type mice (means ± SD). * p < 0.05; ** p < 0.005 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file

    Techniques Used: Infection, Western Blot, Software, Control, Isolation, Expressing

    IL-36β promotes activation of STAT1 and STAT2 during HSV-1 skin infection. a , b Expression of Stat1 ( a ) and Stat2 ( b ) mRNAs were examined in wild type and IL-36β KO HSV-1 infected skin (Fig. ). No statistically significant differences were detected. c Quantification of total STAT1 and pSTAT1 in wild type and IL-36β KO HSV-1 infected skin by western blotting and ImageJ analysis (WT, n = 5; KO, n = 5). d STAT2 and pSTAT2 levels in wild type and IL-36β KO HSV-1 infected skin were determined by western blotting and ImageJ analysis (WT, n = 3; KO, n = 4). c , d Representative data from one of three independent experiments involving male mice is shown. Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file
    Figure Legend Snippet: IL-36β promotes activation of STAT1 and STAT2 during HSV-1 skin infection. a , b Expression of Stat1 ( a ) and Stat2 ( b ) mRNAs were examined in wild type and IL-36β KO HSV-1 infected skin (Fig. ). No statistically significant differences were detected. c Quantification of total STAT1 and pSTAT1 in wild type and IL-36β KO HSV-1 infected skin by western blotting and ImageJ analysis (WT, n = 5; KO, n = 5). d STAT2 and pSTAT2 levels in wild type and IL-36β KO HSV-1 infected skin were determined by western blotting and ImageJ analysis (WT, n = 3; KO, n = 4). c , d Representative data from one of three independent experiments involving male mice is shown. Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file

    Techniques Used: Activation Assay, Infection, Expressing, Western Blot

    STAT1 is activated in epidermal keratinocytes during HSV-1 infection. Wild type and IL-36β KO mice were infected with HSV-1 and skin along the dermatome collected 5 days later. Consecutive skin sections were examined by H&E and pSTAT1 immunohistochemistry. Early ( a – h ), intermediate ( i – p ), and advanced ( q – x ) lesions are shown. Black, blue, and red arrows point to lesion edges and positive pSTAT1 nuclei in keratinocytes and leukocytes, respectively. Black and blue scale bars represent 200 and 50 μm, respectively
    Figure Legend Snippet: STAT1 is activated in epidermal keratinocytes during HSV-1 infection. Wild type and IL-36β KO mice were infected with HSV-1 and skin along the dermatome collected 5 days later. Consecutive skin sections were examined by H&E and pSTAT1 immunohistochemistry. Early ( a – h ), intermediate ( i – p ), and advanced ( q – x ) lesions are shown. Black, blue, and red arrows point to lesion edges and positive pSTAT1 nuclei in keratinocytes and leukocytes, respectively. Black and blue scale bars represent 200 and 50 μm, respectively

    Techniques Used: Infection, Immunohistochemistry

    IL-36β induces STAT1- and STAT2-dependent antiviral immunity in keratinocytes. a Human keratinocytes were pre-treated with medium only or IL-36β before infection with HSV-1 (MOI = 0.01). Levels of HSV-1 ICP4 protein were determined by Western blotting and ImageJ analyses using GAPDH as control. b Mouse primary keratinocytes were pre-treated with medium only or IL-36β, followed by HSV-1 infection (MOI = 0.01), and ICP4 levels examined by western blotting. c Wild type ( + / + ) and IL-36β KO (−/−) mouse primary keratinocytes were infected with 0.01 MOI HSV-1 and ICP4 examined by western blotting. d Wild type and STAT1 −/− primary male mouse keratinocytes were treated with medium only or IL-36β followed by HSV-1 infection (MOI = 0.01) for 24 h. Levels of HSV-1 ICP4 and host Mx1 were examined by western blotting. e Wild type and STAT2 −/− primary male mouse keratinocytes were examined after IL-36β pre-treatment and HSV-1 infection using western blotting. a – e Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group); ** p < 0.01. Each red dot represents a single data point. Source data are provided as a Source Data file
    Figure Legend Snippet: IL-36β induces STAT1- and STAT2-dependent antiviral immunity in keratinocytes. a Human keratinocytes were pre-treated with medium only or IL-36β before infection with HSV-1 (MOI = 0.01). Levels of HSV-1 ICP4 protein were determined by Western blotting and ImageJ analyses using GAPDH as control. b Mouse primary keratinocytes were pre-treated with medium only or IL-36β, followed by HSV-1 infection (MOI = 0.01), and ICP4 levels examined by western blotting. c Wild type ( + / + ) and IL-36β KO (−/−) mouse primary keratinocytes were infected with 0.01 MOI HSV-1 and ICP4 examined by western blotting. d Wild type and STAT1 −/− primary male mouse keratinocytes were treated with medium only or IL-36β followed by HSV-1 infection (MOI = 0.01) for 24 h. Levels of HSV-1 ICP4 and host Mx1 were examined by western blotting. e Wild type and STAT2 −/− primary male mouse keratinocytes were examined after IL-36β pre-treatment and HSV-1 infection using western blotting. a – e Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group); ** p < 0.01. Each red dot represents a single data point. Source data are provided as a Source Data file

    Techniques Used: Infection, Western Blot, Control

    IL-36β activates expression of IFNAR1 and IFNAR2. a Ifnar1 and Ifnar2 mRNA expression was analyzed by real-time PCR in male mouse primary keratinocytes treated with medium only or IL-36β as indicated. b Mouse IFNAR1 and IFNAR2 protein expression was examined by western blotting and ImageJ analyses. c Human keratinocytes were treated with medium only or IL-36β and expression of IFNAR1 and IFNAR2 mRNA determined by real-time PCR. d Expression of human IFNAR1 and IFNAR2 protein was examined by western blotting and ImageJ analyses. a – d Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group); ** p < 0.01. Each red dot represents a single data point. Source data are provided as a Source Data file
    Figure Legend Snippet: IL-36β activates expression of IFNAR1 and IFNAR2. a Ifnar1 and Ifnar2 mRNA expression was analyzed by real-time PCR in male mouse primary keratinocytes treated with medium only or IL-36β as indicated. b Mouse IFNAR1 and IFNAR2 protein expression was examined by western blotting and ImageJ analyses. c Human keratinocytes were treated with medium only or IL-36β and expression of IFNAR1 and IFNAR2 mRNA determined by real-time PCR. d Expression of human IFNAR1 and IFNAR2 protein was examined by western blotting and ImageJ analyses. a – d Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group); ** p < 0.01. Each red dot represents a single data point. Source data are provided as a Source Data file

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Western Blot

    IRF1 is induced by IL-36β and has divergent impact on IFNAR expression. a , b IRF1 mRNA expression in mouse ( a ) and human ( b ) keratinocytes was examined following IL-36β treatment at indicated time-points. c Mouse wild type and IRF1 −/− primary keratinocytes were treated as indicated for 6 h and expression of Ifnar1 and Ifnar2 mRNA analyzed by real-time PCR. d Mouse wild type and IRF1 −/− keratinocytes were treated with medium only or IL-36β for 6 h and IFNAR protein expression examined by western blotting and ImageJ analyses. e IFNAR1 and IFNAR2 mRNA expression in human control (Ctrl) and IRF1 −/− keratinocytes was examined following medium only or IL-36β treatment for 6 h. f Protein levels of IFNAR1 and IFNAR2 in human control and IRF1 −/− keratinocytes were determined by western blotting 6 h post-treatment. a – f Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01; # p > 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file
    Figure Legend Snippet: IRF1 is induced by IL-36β and has divergent impact on IFNAR expression. a , b IRF1 mRNA expression in mouse ( a ) and human ( b ) keratinocytes was examined following IL-36β treatment at indicated time-points. c Mouse wild type and IRF1 −/− primary keratinocytes were treated as indicated for 6 h and expression of Ifnar1 and Ifnar2 mRNA analyzed by real-time PCR. d Mouse wild type and IRF1 −/− keratinocytes were treated with medium only or IL-36β for 6 h and IFNAR protein expression examined by western blotting and ImageJ analyses. e IFNAR1 and IFNAR2 mRNA expression in human control (Ctrl) and IRF1 −/− keratinocytes was examined following medium only or IL-36β treatment for 6 h. f Protein levels of IFNAR1 and IFNAR2 in human control and IRF1 −/− keratinocytes were determined by western blotting 6 h post-treatment. a – f Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01; # p > 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Western Blot, Control

    IRF1 is partially involved in immunity against HSV-1. a – e C57BL/6 J (WT) and IRF1 KO mice were infected with HSV-1 on the flank. a Survival was monitored for 16 days. b Weight was measured for 9 days. c Gastrointestinal dysfunction was examined at day 9 post-infection. Red arrow points to disease affected stomach. d Skin lesion sizes were measured (male mice; WT: n = 5; KO: n = 4). e HSV-1 DNA copy numbers in the skin were determined 6 days post-infection (male mice; WT: n = 7; KO: n = 6). f Mouse primary keratinocytes from wild type (WT) and IRF1 KO mice were sequentially treated with medium only or IL-36β as indicated and infected with HSV-1 ( n = 2 biologically independent samples per treatment group). Levels of ICP4 and Mx1 were evaluated by western blotting and ImageJ analyses. g Levels of ICP4 and Mx1 protein were evaluated by western blotting and ImageJ analyses following IL-36β treatment and HSV-1 infection of human control (Ctrl) and IRF1 KO keratinocytes ( n = 2 biologically independent samples per treatment group). a , c * p < 0.05; ** p < 0.01 (Mantel-Cox and Gehan-Breslow-Wilcoxon tests). d – g Quantitative data are shown as means ± SD. * p < 0.05; # p > 0.05 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file
    Figure Legend Snippet: IRF1 is partially involved in immunity against HSV-1. a – e C57BL/6 J (WT) and IRF1 KO mice were infected with HSV-1 on the flank. a Survival was monitored for 16 days. b Weight was measured for 9 days. c Gastrointestinal dysfunction was examined at day 9 post-infection. Red arrow points to disease affected stomach. d Skin lesion sizes were measured (male mice; WT: n = 5; KO: n = 4). e HSV-1 DNA copy numbers in the skin were determined 6 days post-infection (male mice; WT: n = 7; KO: n = 6). f Mouse primary keratinocytes from wild type (WT) and IRF1 KO mice were sequentially treated with medium only or IL-36β as indicated and infected with HSV-1 ( n = 2 biologically independent samples per treatment group). Levels of ICP4 and Mx1 were evaluated by western blotting and ImageJ analyses. g Levels of ICP4 and Mx1 protein were evaluated by western blotting and ImageJ analyses following IL-36β treatment and HSV-1 infection of human control (Ctrl) and IRF1 KO keratinocytes ( n = 2 biologically independent samples per treatment group). a , c * p < 0.05; ** p < 0.01 (Mantel-Cox and Gehan-Breslow-Wilcoxon tests). d – g Quantitative data are shown as means ± SD. * p < 0.05; # p > 0.05 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file

    Techniques Used: Infection, Western Blot, Control

    IL-36β induced antiviral state is dependent upon IFNAR. a Human keratinocytes were transfected with control (Ctrl) or IFNAR1 gRNA/Cas9 expression plasmids, treated with IL-36β and infected with HSV-1. b Control (Ctrl) or IFNAR2 gRNA/Cas9 expression plasmid transfected human keratinocytes were treated with IL-36β and infected with HSV-1. a , b Levels of ICP4, Mx1, IFNAR1, IFNAR2, and GAPDH were determined using western blotting and ImageJ analyses. c Mouse primary keratinocytes were treated with IL-36β as indicated, incubated with neutralizing antibodies against IFNAR or isotype matched Ig and infected with HSV-1. Levels of ICP4, Mx1 and GAPDH were determined using western blotting and ImageJ analyses. a – c Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file
    Figure Legend Snippet: IL-36β induced antiviral state is dependent upon IFNAR. a Human keratinocytes were transfected with control (Ctrl) or IFNAR1 gRNA/Cas9 expression plasmids, treated with IL-36β and infected with HSV-1. b Control (Ctrl) or IFNAR2 gRNA/Cas9 expression plasmid transfected human keratinocytes were treated with IL-36β and infected with HSV-1. a , b Levels of ICP4, Mx1, IFNAR1, IFNAR2, and GAPDH were determined using western blotting and ImageJ analyses. c Mouse primary keratinocytes were treated with IL-36β as indicated, incubated with neutralizing antibodies against IFNAR or isotype matched Ig and infected with HSV-1. Levels of ICP4, Mx1 and GAPDH were determined using western blotting and ImageJ analyses. a – c Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file

    Techniques Used: Transfection, Control, Expressing, Infection, Plasmid Preparation, Western Blot, Incubation

    IL-36β accelerates type I IFN signaling. Medium only or IL-36β treated keratinocytes were further treated with type I IFN (0.01 ng mL −1 ) as indicated. Phosphorylation of STAT1 and STAT2 was examined by western blotting and ImageJ analyses. Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). a Human keratinocytes were analyzed. b Mouse primary keratinocytes were examined. Each red dot represents a single data point. Source data are provided as a Source Data file
    Figure Legend Snippet: IL-36β accelerates type I IFN signaling. Medium only or IL-36β treated keratinocytes were further treated with type I IFN (0.01 ng mL −1 ) as indicated. Phosphorylation of STAT1 and STAT2 was examined by western blotting and ImageJ analyses. Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). a Human keratinocytes were analyzed. b Mouse primary keratinocytes were examined. Each red dot represents a single data point. Source data are provided as a Source Data file

    Techniques Used: Phospho-proteomics, Western Blot

    IL-1 promotes enhanced type I IFN signaling through IFNAR in human cells. a , b Gene editing was performed in human keratinocytes using control (Ctrl), IFNAR1 ( a ) or IFNAR2 ( b ) gRNAs and Cas9. Cells were treated with medium only or IL-36β, infected with HSV-1 and analyzed by western blotting. c Cells were pre-treated with medium only or IL-1α followed by IFN-α/β. STAT1/2 activation was examined by western blotting. Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file
    Figure Legend Snippet: IL-1 promotes enhanced type I IFN signaling through IFNAR in human cells. a , b Gene editing was performed in human keratinocytes using control (Ctrl), IFNAR1 ( a ) or IFNAR2 ( b ) gRNAs and Cas9. Cells were treated with medium only or IL-36β, infected with HSV-1 and analyzed by western blotting. c Cells were pre-treated with medium only or IL-1α followed by IFN-α/β. STAT1/2 activation was examined by western blotting. Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file

    Techniques Used: Control, Infection, Western Blot, Activation Assay



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    IL-36β KO mice exhibit altered responses to HSV-1 skin infection. a Wild type (WT; n = 5 ♀ and 13 ♂) and IL-36β KO mice ( n = 7 ♀ and 12 ♂) were infected with HSV-1 on the flank and skin regions along HSV-1 infected dermatomes collected 6 days post-infection. Viral DNA loads were determined by QPCR. Data are pooled from three independent experiments and shown as means ( ± SD). * p < 0.05 (One-Way ANOVA). b , c Viral ICP4 protein levels were examined by Western blotting ( b ) and quantified using ImageJ software ( c ). GAPDH was used as loading control. Data are representative of three independent experiments and shown as means (±SD) in c (WT: n = 2 female and 4 male; IL-36β KO mice: n = 3 female and 3 male). * p < 0.05 (one-way ANOVA). d Wild type and IL - 36β KO mice were infected with HSV-1 ( n = 3 per group) on the flank and skin RNA isolated 6 days post-infection. Heat-map of genes differentially expressed in the two strains is shown. e Pathway associations of genes identified as differentially expressed in d . f Expression of Oas1 , Eif2ak2, Isg15, Ifitm3, Ifitm2, and Ifit3 mRNAs were examined in wild type and IL-36β KO HSV-1 infected skin ( a ). The mRNAs were normalized against GAPDH and are shown as relative expression compared to female wild-type mice (means ± SD). * p < 0.05; ** p < 0.005 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file

    Journal: Nature Communications

    Article Title: IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners

    doi: 10.1038/s41467-019-12318-y

    Figure Lengend Snippet: IL-36β KO mice exhibit altered responses to HSV-1 skin infection. a Wild type (WT; n = 5 ♀ and 13 ♂) and IL-36β KO mice ( n = 7 ♀ and 12 ♂) were infected with HSV-1 on the flank and skin regions along HSV-1 infected dermatomes collected 6 days post-infection. Viral DNA loads were determined by QPCR. Data are pooled from three independent experiments and shown as means ( ± SD). * p < 0.05 (One-Way ANOVA). b , c Viral ICP4 protein levels were examined by Western blotting ( b ) and quantified using ImageJ software ( c ). GAPDH was used as loading control. Data are representative of three independent experiments and shown as means (±SD) in c (WT: n = 2 female and 4 male; IL-36β KO mice: n = 3 female and 3 male). * p < 0.05 (one-way ANOVA). d Wild type and IL - 36β KO mice were infected with HSV-1 ( n = 3 per group) on the flank and skin RNA isolated 6 days post-infection. Heat-map of genes differentially expressed in the two strains is shown. e Pathway associations of genes identified as differentially expressed in d . f Expression of Oas1 , Eif2ak2, Isg15, Ifitm3, Ifitm2, and Ifit3 mRNAs were examined in wild type and IL-36β KO HSV-1 infected skin ( a ). The mRNAs were normalized against GAPDH and are shown as relative expression compared to female wild-type mice (means ± SD). * p < 0.05; ** p < 0.005 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file

    Article Snippet: Recombinant human IL-36β (Catalog #: 6834-ILB-025), mouse IL-36β (Catalog #: 7060-ML-010) protein, and Universal Type I IFN (Catalog #: 11200–1) were obtained from R&D Systems.

    Techniques: Infection, Western Blot, Software, Control, Isolation, Expressing

    IL-36β promotes activation of STAT1 and STAT2 during HSV-1 skin infection. a , b Expression of Stat1 ( a ) and Stat2 ( b ) mRNAs were examined in wild type and IL-36β KO HSV-1 infected skin (Fig. ). No statistically significant differences were detected. c Quantification of total STAT1 and pSTAT1 in wild type and IL-36β KO HSV-1 infected skin by western blotting and ImageJ analysis (WT, n = 5; KO, n = 5). d STAT2 and pSTAT2 levels in wild type and IL-36β KO HSV-1 infected skin were determined by western blotting and ImageJ analysis (WT, n = 3; KO, n = 4). c , d Representative data from one of three independent experiments involving male mice is shown. Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file

    Journal: Nature Communications

    Article Title: IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners

    doi: 10.1038/s41467-019-12318-y

    Figure Lengend Snippet: IL-36β promotes activation of STAT1 and STAT2 during HSV-1 skin infection. a , b Expression of Stat1 ( a ) and Stat2 ( b ) mRNAs were examined in wild type and IL-36β KO HSV-1 infected skin (Fig. ). No statistically significant differences were detected. c Quantification of total STAT1 and pSTAT1 in wild type and IL-36β KO HSV-1 infected skin by western blotting and ImageJ analysis (WT, n = 5; KO, n = 5). d STAT2 and pSTAT2 levels in wild type and IL-36β KO HSV-1 infected skin were determined by western blotting and ImageJ analysis (WT, n = 3; KO, n = 4). c , d Representative data from one of three independent experiments involving male mice is shown. Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file

    Article Snippet: Recombinant human IL-36β (Catalog #: 6834-ILB-025), mouse IL-36β (Catalog #: 7060-ML-010) protein, and Universal Type I IFN (Catalog #: 11200–1) were obtained from R&D Systems.

    Techniques: Activation Assay, Infection, Expressing, Western Blot

    STAT1 is activated in epidermal keratinocytes during HSV-1 infection. Wild type and IL-36β KO mice were infected with HSV-1 and skin along the dermatome collected 5 days later. Consecutive skin sections were examined by H&E and pSTAT1 immunohistochemistry. Early ( a – h ), intermediate ( i – p ), and advanced ( q – x ) lesions are shown. Black, blue, and red arrows point to lesion edges and positive pSTAT1 nuclei in keratinocytes and leukocytes, respectively. Black and blue scale bars represent 200 and 50 μm, respectively

    Journal: Nature Communications

    Article Title: IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners

    doi: 10.1038/s41467-019-12318-y

    Figure Lengend Snippet: STAT1 is activated in epidermal keratinocytes during HSV-1 infection. Wild type and IL-36β KO mice were infected with HSV-1 and skin along the dermatome collected 5 days later. Consecutive skin sections were examined by H&E and pSTAT1 immunohistochemistry. Early ( a – h ), intermediate ( i – p ), and advanced ( q – x ) lesions are shown. Black, blue, and red arrows point to lesion edges and positive pSTAT1 nuclei in keratinocytes and leukocytes, respectively. Black and blue scale bars represent 200 and 50 μm, respectively

    Article Snippet: Recombinant human IL-36β (Catalog #: 6834-ILB-025), mouse IL-36β (Catalog #: 7060-ML-010) protein, and Universal Type I IFN (Catalog #: 11200–1) were obtained from R&D Systems.

    Techniques: Infection, Immunohistochemistry

    IL-36β induces STAT1- and STAT2-dependent antiviral immunity in keratinocytes. a Human keratinocytes were pre-treated with medium only or IL-36β before infection with HSV-1 (MOI = 0.01). Levels of HSV-1 ICP4 protein were determined by Western blotting and ImageJ analyses using GAPDH as control. b Mouse primary keratinocytes were pre-treated with medium only or IL-36β, followed by HSV-1 infection (MOI = 0.01), and ICP4 levels examined by western blotting. c Wild type ( + / + ) and IL-36β KO (−/−) mouse primary keratinocytes were infected with 0.01 MOI HSV-1 and ICP4 examined by western blotting. d Wild type and STAT1 −/− primary male mouse keratinocytes were treated with medium only or IL-36β followed by HSV-1 infection (MOI = 0.01) for 24 h. Levels of HSV-1 ICP4 and host Mx1 were examined by western blotting. e Wild type and STAT2 −/− primary male mouse keratinocytes were examined after IL-36β pre-treatment and HSV-1 infection using western blotting. a – e Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group); ** p < 0.01. Each red dot represents a single data point. Source data are provided as a Source Data file

    Journal: Nature Communications

    Article Title: IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners

    doi: 10.1038/s41467-019-12318-y

    Figure Lengend Snippet: IL-36β induces STAT1- and STAT2-dependent antiviral immunity in keratinocytes. a Human keratinocytes were pre-treated with medium only or IL-36β before infection with HSV-1 (MOI = 0.01). Levels of HSV-1 ICP4 protein were determined by Western blotting and ImageJ analyses using GAPDH as control. b Mouse primary keratinocytes were pre-treated with medium only or IL-36β, followed by HSV-1 infection (MOI = 0.01), and ICP4 levels examined by western blotting. c Wild type ( + / + ) and IL-36β KO (−/−) mouse primary keratinocytes were infected with 0.01 MOI HSV-1 and ICP4 examined by western blotting. d Wild type and STAT1 −/− primary male mouse keratinocytes were treated with medium only or IL-36β followed by HSV-1 infection (MOI = 0.01) for 24 h. Levels of HSV-1 ICP4 and host Mx1 were examined by western blotting. e Wild type and STAT2 −/− primary male mouse keratinocytes were examined after IL-36β pre-treatment and HSV-1 infection using western blotting. a – e Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group); ** p < 0.01. Each red dot represents a single data point. Source data are provided as a Source Data file

    Article Snippet: Recombinant human IL-36β (Catalog #: 6834-ILB-025), mouse IL-36β (Catalog #: 7060-ML-010) protein, and Universal Type I IFN (Catalog #: 11200–1) were obtained from R&D Systems.

    Techniques: Infection, Western Blot, Control

    IL-36β activates expression of IFNAR1 and IFNAR2. a Ifnar1 and Ifnar2 mRNA expression was analyzed by real-time PCR in male mouse primary keratinocytes treated with medium only or IL-36β as indicated. b Mouse IFNAR1 and IFNAR2 protein expression was examined by western blotting and ImageJ analyses. c Human keratinocytes were treated with medium only or IL-36β and expression of IFNAR1 and IFNAR2 mRNA determined by real-time PCR. d Expression of human IFNAR1 and IFNAR2 protein was examined by western blotting and ImageJ analyses. a – d Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group); ** p < 0.01. Each red dot represents a single data point. Source data are provided as a Source Data file

    Journal: Nature Communications

    Article Title: IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners

    doi: 10.1038/s41467-019-12318-y

    Figure Lengend Snippet: IL-36β activates expression of IFNAR1 and IFNAR2. a Ifnar1 and Ifnar2 mRNA expression was analyzed by real-time PCR in male mouse primary keratinocytes treated with medium only or IL-36β as indicated. b Mouse IFNAR1 and IFNAR2 protein expression was examined by western blotting and ImageJ analyses. c Human keratinocytes were treated with medium only or IL-36β and expression of IFNAR1 and IFNAR2 mRNA determined by real-time PCR. d Expression of human IFNAR1 and IFNAR2 protein was examined by western blotting and ImageJ analyses. a – d Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group); ** p < 0.01. Each red dot represents a single data point. Source data are provided as a Source Data file

    Article Snippet: Recombinant human IL-36β (Catalog #: 6834-ILB-025), mouse IL-36β (Catalog #: 7060-ML-010) protein, and Universal Type I IFN (Catalog #: 11200–1) were obtained from R&D Systems.

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot

    IRF1 is induced by IL-36β and has divergent impact on IFNAR expression. a , b IRF1 mRNA expression in mouse ( a ) and human ( b ) keratinocytes was examined following IL-36β treatment at indicated time-points. c Mouse wild type and IRF1 −/− primary keratinocytes were treated as indicated for 6 h and expression of Ifnar1 and Ifnar2 mRNA analyzed by real-time PCR. d Mouse wild type and IRF1 −/− keratinocytes were treated with medium only or IL-36β for 6 h and IFNAR protein expression examined by western blotting and ImageJ analyses. e IFNAR1 and IFNAR2 mRNA expression in human control (Ctrl) and IRF1 −/− keratinocytes was examined following medium only or IL-36β treatment for 6 h. f Protein levels of IFNAR1 and IFNAR2 in human control and IRF1 −/− keratinocytes were determined by western blotting 6 h post-treatment. a – f Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01; # p > 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file

    Journal: Nature Communications

    Article Title: IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners

    doi: 10.1038/s41467-019-12318-y

    Figure Lengend Snippet: IRF1 is induced by IL-36β and has divergent impact on IFNAR expression. a , b IRF1 mRNA expression in mouse ( a ) and human ( b ) keratinocytes was examined following IL-36β treatment at indicated time-points. c Mouse wild type and IRF1 −/− primary keratinocytes were treated as indicated for 6 h and expression of Ifnar1 and Ifnar2 mRNA analyzed by real-time PCR. d Mouse wild type and IRF1 −/− keratinocytes were treated with medium only or IL-36β for 6 h and IFNAR protein expression examined by western blotting and ImageJ analyses. e IFNAR1 and IFNAR2 mRNA expression in human control (Ctrl) and IRF1 −/− keratinocytes was examined following medium only or IL-36β treatment for 6 h. f Protein levels of IFNAR1 and IFNAR2 in human control and IRF1 −/− keratinocytes were determined by western blotting 6 h post-treatment. a – f Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01; # p > 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file

    Article Snippet: Recombinant human IL-36β (Catalog #: 6834-ILB-025), mouse IL-36β (Catalog #: 7060-ML-010) protein, and Universal Type I IFN (Catalog #: 11200–1) were obtained from R&D Systems.

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot, Control

    IRF1 is partially involved in immunity against HSV-1. a – e C57BL/6 J (WT) and IRF1 KO mice were infected with HSV-1 on the flank. a Survival was monitored for 16 days. b Weight was measured for 9 days. c Gastrointestinal dysfunction was examined at day 9 post-infection. Red arrow points to disease affected stomach. d Skin lesion sizes were measured (male mice; WT: n = 5; KO: n = 4). e HSV-1 DNA copy numbers in the skin were determined 6 days post-infection (male mice; WT: n = 7; KO: n = 6). f Mouse primary keratinocytes from wild type (WT) and IRF1 KO mice were sequentially treated with medium only or IL-36β as indicated and infected with HSV-1 ( n = 2 biologically independent samples per treatment group). Levels of ICP4 and Mx1 were evaluated by western blotting and ImageJ analyses. g Levels of ICP4 and Mx1 protein were evaluated by western blotting and ImageJ analyses following IL-36β treatment and HSV-1 infection of human control (Ctrl) and IRF1 KO keratinocytes ( n = 2 biologically independent samples per treatment group). a , c * p < 0.05; ** p < 0.01 (Mantel-Cox and Gehan-Breslow-Wilcoxon tests). d – g Quantitative data are shown as means ± SD. * p < 0.05; # p > 0.05 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file

    Journal: Nature Communications

    Article Title: IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners

    doi: 10.1038/s41467-019-12318-y

    Figure Lengend Snippet: IRF1 is partially involved in immunity against HSV-1. a – e C57BL/6 J (WT) and IRF1 KO mice were infected with HSV-1 on the flank. a Survival was monitored for 16 days. b Weight was measured for 9 days. c Gastrointestinal dysfunction was examined at day 9 post-infection. Red arrow points to disease affected stomach. d Skin lesion sizes were measured (male mice; WT: n = 5; KO: n = 4). e HSV-1 DNA copy numbers in the skin were determined 6 days post-infection (male mice; WT: n = 7; KO: n = 6). f Mouse primary keratinocytes from wild type (WT) and IRF1 KO mice were sequentially treated with medium only or IL-36β as indicated and infected with HSV-1 ( n = 2 biologically independent samples per treatment group). Levels of ICP4 and Mx1 were evaluated by western blotting and ImageJ analyses. g Levels of ICP4 and Mx1 protein were evaluated by western blotting and ImageJ analyses following IL-36β treatment and HSV-1 infection of human control (Ctrl) and IRF1 KO keratinocytes ( n = 2 biologically independent samples per treatment group). a , c * p < 0.05; ** p < 0.01 (Mantel-Cox and Gehan-Breslow-Wilcoxon tests). d – g Quantitative data are shown as means ± SD. * p < 0.05; # p > 0.05 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file

    Article Snippet: Recombinant human IL-36β (Catalog #: 6834-ILB-025), mouse IL-36β (Catalog #: 7060-ML-010) protein, and Universal Type I IFN (Catalog #: 11200–1) were obtained from R&D Systems.

    Techniques: Infection, Western Blot, Control

    IL-36β induced antiviral state is dependent upon IFNAR. a Human keratinocytes were transfected with control (Ctrl) or IFNAR1 gRNA/Cas9 expression plasmids, treated with IL-36β and infected with HSV-1. b Control (Ctrl) or IFNAR2 gRNA/Cas9 expression plasmid transfected human keratinocytes were treated with IL-36β and infected with HSV-1. a , b Levels of ICP4, Mx1, IFNAR1, IFNAR2, and GAPDH were determined using western blotting and ImageJ analyses. c Mouse primary keratinocytes were treated with IL-36β as indicated, incubated with neutralizing antibodies against IFNAR or isotype matched Ig and infected with HSV-1. Levels of ICP4, Mx1 and GAPDH were determined using western blotting and ImageJ analyses. a – c Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file

    Journal: Nature Communications

    Article Title: IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners

    doi: 10.1038/s41467-019-12318-y

    Figure Lengend Snippet: IL-36β induced antiviral state is dependent upon IFNAR. a Human keratinocytes were transfected with control (Ctrl) or IFNAR1 gRNA/Cas9 expression plasmids, treated with IL-36β and infected with HSV-1. b Control (Ctrl) or IFNAR2 gRNA/Cas9 expression plasmid transfected human keratinocytes were treated with IL-36β and infected with HSV-1. a , b Levels of ICP4, Mx1, IFNAR1, IFNAR2, and GAPDH were determined using western blotting and ImageJ analyses. c Mouse primary keratinocytes were treated with IL-36β as indicated, incubated with neutralizing antibodies against IFNAR or isotype matched Ig and infected with HSV-1. Levels of ICP4, Mx1 and GAPDH were determined using western blotting and ImageJ analyses. a – c Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file

    Article Snippet: Recombinant human IL-36β (Catalog #: 6834-ILB-025), mouse IL-36β (Catalog #: 7060-ML-010) protein, and Universal Type I IFN (Catalog #: 11200–1) were obtained from R&D Systems.

    Techniques: Transfection, Control, Expressing, Infection, Plasmid Preparation, Western Blot, Incubation

    IL-36β accelerates type I IFN signaling. Medium only or IL-36β treated keratinocytes were further treated with type I IFN (0.01 ng mL −1 ) as indicated. Phosphorylation of STAT1 and STAT2 was examined by western blotting and ImageJ analyses. Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). a Human keratinocytes were analyzed. b Mouse primary keratinocytes were examined. Each red dot represents a single data point. Source data are provided as a Source Data file

    Journal: Nature Communications

    Article Title: IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners

    doi: 10.1038/s41467-019-12318-y

    Figure Lengend Snippet: IL-36β accelerates type I IFN signaling. Medium only or IL-36β treated keratinocytes were further treated with type I IFN (0.01 ng mL −1 ) as indicated. Phosphorylation of STAT1 and STAT2 was examined by western blotting and ImageJ analyses. Quantitative data are shown as means ± SD. * p < 0.05 (one-way ANOVA, n = 2 biologically independent samples per treatment group). a Human keratinocytes were analyzed. b Mouse primary keratinocytes were examined. Each red dot represents a single data point. Source data are provided as a Source Data file

    Article Snippet: Recombinant human IL-36β (Catalog #: 6834-ILB-025), mouse IL-36β (Catalog #: 7060-ML-010) protein, and Universal Type I IFN (Catalog #: 11200–1) were obtained from R&D Systems.

    Techniques: Phospho-proteomics, Western Blot

    IL-1 promotes enhanced type I IFN signaling through IFNAR in human cells. a , b Gene editing was performed in human keratinocytes using control (Ctrl), IFNAR1 ( a ) or IFNAR2 ( b ) gRNAs and Cas9. Cells were treated with medium only or IL-36β, infected with HSV-1 and analyzed by western blotting. c Cells were pre-treated with medium only or IL-1α followed by IFN-α/β. STAT1/2 activation was examined by western blotting. Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file

    Journal: Nature Communications

    Article Title: IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners

    doi: 10.1038/s41467-019-12318-y

    Figure Lengend Snippet: IL-1 promotes enhanced type I IFN signaling through IFNAR in human cells. a , b Gene editing was performed in human keratinocytes using control (Ctrl), IFNAR1 ( a ) or IFNAR2 ( b ) gRNAs and Cas9. Cells were treated with medium only or IL-36β, infected with HSV-1 and analyzed by western blotting. c Cells were pre-treated with medium only or IL-1α followed by IFN-α/β. STAT1/2 activation was examined by western blotting. Quantitative data are shown as means ± SD. * p < 0.05; ** p < 0.01 (one-way ANOVA, n = 2 biologically independent samples per treatment group). Each red dot represents a single data point. Source data are provided as a Source Data file

    Article Snippet: Recombinant human IL-36β (Catalog #: 6834-ILB-025), mouse IL-36β (Catalog #: 7060-ML-010) protein, and Universal Type I IFN (Catalog #: 11200–1) were obtained from R&D Systems.

    Techniques: Control, Infection, Western Blot, Activation Assay

    Microarray gene profiling identifies overexpressed IL-36 family members in ONJ-like lesions in mice. (A) A graphic representation of timeline used in this study. (B) Clinical illustration of the osteomucosal tissues before and after removal at the tooth-extracted areas photographed 2 weeks after tooth extraction. (C) A graphic representation of the microarray profiling that are differentially expressed more than fivefold were represented (n = 3 per group). (D) The ingenuity pathway analysis (IPA) of functional pathways that are associated with ONJ lesions. (E) Lists of genes involved in biosynthesis of steroids. (F) List of genes involved in role of osteoblasts, osteoclasts, and chondrocytes in rheumatoid arthritis. The unhealed osteomucosal tissues at the tooth-extracted sites were harvested and subjected mRNA isolation, cDNA synthesis, and qRT-PCR for (G) IL-18, (H) IL-36α, (I) IL-36β, (J) IL-36γ, and (K) FDPS. The results are from two independent non-BRONJ and BRONJ lesions. (L) Staining for H&E and IHC staining for IL-36α at the tooth-extracted sites in vehicle (Veh)- or Zometa (ZOL)-treated mice. Scale bar = 100 µm. ELISA for (M) IL-18 and (N) IL-36α from the serum obtained from Veh- or ZOL-treated mice 2 weeks after tooth extraction. *p<0.05; **p<0.01; ***p<0.001. Results represent the means ± SD performed in triplicate unless otherwise indicated.

    Journal: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

    Article Title: IL-36 Induces Bisphosphonate-Related Osteonecrosis of the Jaw-Like Lesions in Mice by Inhibiting TGF-β-Mediated Collagen Expression

    doi: 10.1002/jbmr.2985

    Figure Lengend Snippet: Microarray gene profiling identifies overexpressed IL-36 family members in ONJ-like lesions in mice. (A) A graphic representation of timeline used in this study. (B) Clinical illustration of the osteomucosal tissues before and after removal at the tooth-extracted areas photographed 2 weeks after tooth extraction. (C) A graphic representation of the microarray profiling that are differentially expressed more than fivefold were represented (n = 3 per group). (D) The ingenuity pathway analysis (IPA) of functional pathways that are associated with ONJ lesions. (E) Lists of genes involved in biosynthesis of steroids. (F) List of genes involved in role of osteoblasts, osteoclasts, and chondrocytes in rheumatoid arthritis. The unhealed osteomucosal tissues at the tooth-extracted sites were harvested and subjected mRNA isolation, cDNA synthesis, and qRT-PCR for (G) IL-18, (H) IL-36α, (I) IL-36β, (J) IL-36γ, and (K) FDPS. The results are from two independent non-BRONJ and BRONJ lesions. (L) Staining for H&E and IHC staining for IL-36α at the tooth-extracted sites in vehicle (Veh)- or Zometa (ZOL)-treated mice. Scale bar = 100 µm. ELISA for (M) IL-18 and (N) IL-36α from the serum obtained from Veh- or ZOL-treated mice 2 weeks after tooth extraction. *p<0.05; **p<0.01; ***p<0.001. Results represent the means ± SD performed in triplicate unless otherwise indicated.

    Article Snippet: Recombinant IL-36α (7059-ML), IL-36β (7060-ML), IL-36γ (6996-ML), and TGF-β (7666-MB) were obtained from R&D Systems (Minneapolis, MN, USA).

    Techniques: Microarray, Extraction, Functional Assay, Isolation, cDNA Synthesis, Quantitative RT-PCR, Staining, Immunohistochemistry, Enzyme-linked Immunosorbent Assay

    IL-36α inhibits expression of collagen and α-Sma in GMSCs. (A) List of genes associated with connective tissues (eg, collagenous and non-collagenous proteins) from the microarray data. (B) qRT-PCR of Il-6 in gingival mesenchymal stem cells (GMSCs) treated with recombinant IL-36α, IL-36β, and IL-36γ for 4 days. (C) qRT-PCR of Col1a1, Col1a2, and Col3a1 in GMSCs treated with recombinant IL-36α, IL-36β, and IL-36γ for 4 days. (D) Western blotting of IL-1Rrp2 after knocking down with control siRNA (CTLsi) or IL-1Rrp2 siRNA (IL-1Rrp2si) in GMSCs. (E) qRT-PCR of Col1a1, Col1a2, and Col3a1 in GMSCs with IL-1Rrp2 knockdown and IL-36a treatment. (F) Western blotting of Col1a1 and α-Sma in GMSCs treated with IL-36α and TGF-β1 for 2 days. (G) ELISA for collagen type I from supernatants obtained from GMSCs treated with IL-36α and TGF-β1. (H) qRT-PCR of Col1a1, Col1a2, and α-Sma in GMSCs treated with recombinant IL-36α and TGF-β1 for 2 days. *p<0.05; **p<0.01; ***p<0.001. Results represent the means ± SD performed in triplicate.

    Journal: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

    Article Title: IL-36 Induces Bisphosphonate-Related Osteonecrosis of the Jaw-Like Lesions in Mice by Inhibiting TGF-β-Mediated Collagen Expression

    doi: 10.1002/jbmr.2985

    Figure Lengend Snippet: IL-36α inhibits expression of collagen and α-Sma in GMSCs. (A) List of genes associated with connective tissues (eg, collagenous and non-collagenous proteins) from the microarray data. (B) qRT-PCR of Il-6 in gingival mesenchymal stem cells (GMSCs) treated with recombinant IL-36α, IL-36β, and IL-36γ for 4 days. (C) qRT-PCR of Col1a1, Col1a2, and Col3a1 in GMSCs treated with recombinant IL-36α, IL-36β, and IL-36γ for 4 days. (D) Western blotting of IL-1Rrp2 after knocking down with control siRNA (CTLsi) or IL-1Rrp2 siRNA (IL-1Rrp2si) in GMSCs. (E) qRT-PCR of Col1a1, Col1a2, and Col3a1 in GMSCs with IL-1Rrp2 knockdown and IL-36a treatment. (F) Western blotting of Col1a1 and α-Sma in GMSCs treated with IL-36α and TGF-β1 for 2 days. (G) ELISA for collagen type I from supernatants obtained from GMSCs treated with IL-36α and TGF-β1. (H) qRT-PCR of Col1a1, Col1a2, and α-Sma in GMSCs treated with recombinant IL-36α and TGF-β1 for 2 days. *p<0.05; **p<0.01; ***p<0.001. Results represent the means ± SD performed in triplicate.

    Article Snippet: Recombinant IL-36α (7059-ML), IL-36β (7060-ML), IL-36γ (6996-ML), and TGF-β (7666-MB) were obtained from R&D Systems (Minneapolis, MN, USA).

    Techniques: Expressing, Microarray, Quantitative RT-PCR, Recombinant, Western Blot, Control, Knockdown, Enzyme-linked Immunosorbent Assay

    Proposed model. TGF-β1 binds TGF-β receptor and causes phosphorylation of Smad2/3, which in turns translocates into the nucleus and activates the target genes such as Col1a1 or α-Sma. IL-36α binds to IL-36 receptor complex and activates the ERK signaling pathway. Activated Erk inhibits translocation of TGF-β1-activated Smad complex, thereby suppressing the Smad-mediated activation of gene expression.

    Journal: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

    Article Title: IL-36 Induces Bisphosphonate-Related Osteonecrosis of the Jaw-Like Lesions in Mice by Inhibiting TGF-β-Mediated Collagen Expression

    doi: 10.1002/jbmr.2985

    Figure Lengend Snippet: Proposed model. TGF-β1 binds TGF-β receptor and causes phosphorylation of Smad2/3, which in turns translocates into the nucleus and activates the target genes such as Col1a1 or α-Sma. IL-36α binds to IL-36 receptor complex and activates the ERK signaling pathway. Activated Erk inhibits translocation of TGF-β1-activated Smad complex, thereby suppressing the Smad-mediated activation of gene expression.

    Article Snippet: Recombinant IL-36α (7059-ML), IL-36β (7060-ML), IL-36γ (6996-ML), and TGF-β (7666-MB) were obtained from R&D Systems (Minneapolis, MN, USA).

    Techniques: Phospho-proteomics, Translocation Assay, Activation Assay, Gene Expression