il 36β  (R&D Systems)

Journal: International journal of molecular sciences

Article Title: Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis.

doi: 10.3390/ijms241311104

Figure Lengend Snippet: Figure 1. IL-36β is overexpressed on epidermal keratinocytes in lesional skin of atopic dermatitis (AD). (A,B) IL-36β staining in healthy skin and AD lesional skin (n = 10, respectively). Representative images of IL-36β staining in AD skin (A) and in healthy skin (B) are shown (original magnification ×400). Arrows point to representative keratinocytes with the nuclear staining. (C) Double staining of IL-36β (red) and cytokeratin (brown) in AD lesional skin (n = 10). Representative image is shown. Arrows point to representative keratinocytes with nuclear IL-36β staining and cytokeratin staining. (D) IL-36β staining intensity is shown. The measured values from individual patients are plotted by dots. * p < 0.05.

Article Snippet: Simultaneously, the recombinant human IL-36β protein (R&D systems, Minneapolis, MN, USA) were added, and the cells were incubated at 37 ◦C and 5% CO2.

Techniques: Staining, Double Staining

Journal: International journal of molecular sciences

Article Title: Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis.

doi: 10.3390/ijms241311104

Figure Lengend Snippet: Figure 2. Serum IL-36β levels are not elevated in patients with atopic dermatitis (AD) but decreased by dupilumab. (A) Serum IL-36β levels in AD patients (n = 36) and healthy control (n = 15). (B) Serum IL-36β levels in severe AD patients (n = 16) and mild/moderate AD patients (n = 20). (C) Serum IL-36β levels in AD patients (n = 7) before and after dupilumab treatment. The measured values from individual patients are plotted by dots. Bars represent the median. * p < 0.05.

Article Snippet: Simultaneously, the recombinant human IL-36β protein (R&D systems, Minneapolis, MN, USA) were added, and the cells were incubated at 37 ◦C and 5% CO2.

Techniques: Control

Journal: International journal of molecular sciences

Article Title: Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis.

doi: 10.3390/ijms241311104

Figure Lengend Snippet: Figure 3. IL-36β promotes vascular endothelial growth factor (VEGF)-A and placental growth factor (PlGF) mRNA expression in HaCaT cells. (A,B) HaCaT were cultured with recombinant IL-36β (0, 100 ng/mL) for 24 h. Messenger RNA levels of the indicated Th2 cytokines and chemokines (A) and angiogenic factors (B) were determined by quantitative RT-PCR. One representative result from three independent experiments. The measured values from individual samples are plotted by dots. Bars represent the median. (n = 4–6). * p < 0.05.

Article Snippet: Simultaneously, the recombinant human IL-36β protein (R&D systems, Minneapolis, MN, USA) were added, and the cells were incubated at 37 ◦C and 5% CO2.

Techniques: Expressing, Cell Culture, Recombinant, Quantitative RT-PCR

Journal: International journal of molecular sciences

Article Title: Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis.

doi: 10.3390/ijms241311104

Figure Lengend Snippet: Figure 4. IL-36β enhances vascular endothelial growth factor (VEGF)-A protein production via extracellular signal-regulated kinase (ERK)-1/2 pathway from HaCaT cells. (A) HaCaT cells were cultured with recombinant IL-36β (0, 50, 100 ng/mL) for 24 h. Supernatant IL-36β levels were evaluated by enzyme-linked immunosorbent assay. (B) HaCaT cells were cultured with recombinant IL-36β (100 ng/mL) for 24 h in the absence or after preincubation with U0126 (20 nM), LY294002 (20 nM), SB203580 (20 nM), or sc-514 (40 nM). Supernatant IL-36β levels were evaluated by enzyme- linked immunosorbent assay. One representative result from three independent experiments. The measured values from individual samples are plotted by dots. Bars represent the median. (n = 6). * p < 0.05. ** p < 0.01.

Article Snippet: Simultaneously, the recombinant human IL-36β protein (R&D systems, Minneapolis, MN, USA) were added, and the cells were incubated at 37 ◦C and 5% CO2.

Techniques: Cell Culture, Recombinant, Enzyme-linked Immunosorbent Assay

Journal: International journal of molecular sciences

Article Title: Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis.

doi: 10.3390/ijms241311104

Figure Lengend Snippet: Figure 5. IL-36β staining intensity in epidermal keratinocytes is correlated with the number of dermal vessels in lesional skin with atopic dermatitis (AD). (A–D) Vascular endothelial growth factor (VEGF)-A (A,B) and plancental growth factor (PlGF) (C,D) staining in healthy skin and AD lesional skin (n = 10, respectively). Representative images of VEGF-A and PlGF staining in AD skin (A,C), and in healthy skin (B,D) are shown (original magnification ×400). Arrows point to representative keratinocytes with the nuclear staining. (E,F) Double staining of IL-36β (red) and CD34 (brown) in AD lesional skin (n = 10). Representative images of AD skin with relatively few dermal vessels (E) and with relatively abundant dermal vessels (F) are shown (original magnification ×200). (G) The correlation between IL-36β staining intensity and the number of CD34-positive dermal vessels (n = 10). The measured values from individual patients are plotted by dots.

Article Snippet: Simultaneously, the recombinant human IL-36β protein (R&D systems, Minneapolis, MN, USA) were added, and the cells were incubated at 37 ◦C and 5% CO2.

Techniques: Staining, Double Staining

Journal: International Journal of Molecular Sciences

Article Title: Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis

doi: 10.3390/ijms241311104

Figure Lengend Snippet: IL-36β is overexpressed on epidermal keratinocytes in lesional skin of atopic dermatitis (AD). ( A , B ) IL-36β staining in healthy skin and AD lesional skin ( n = 10, respectively). Representative images of IL-36β staining in AD skin ( A ) and in healthy skin ( B ) are shown (original magnification ×400). Arrows point to representative keratinocytes with the nuclear staining. ( C ) Double staining of IL-36β (red) and cytokeratin (brown) in AD lesional skin ( n = 10). Representative image is shown. Arrows point to representative keratinocytes with nuclear IL-36β staining and cytokeratin staining. ( D ) IL-36β staining intensity is shown. The measured values from individual patients are plotted by dots. * p < 0.05.

Article Snippet: Simultaneously, the recombinant human IL-36β protein (R&D systems, Minneapolis, MN, USA) were added, and the cells were incubated at 37 °C and 5% CO 2 .

Techniques: Staining, Double Staining

Journal: International Journal of Molecular Sciences

Article Title: Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis

doi: 10.3390/ijms241311104

Figure Lengend Snippet: Serum IL-36β levels are not elevated in patients with atopic dermatitis (AD) but decreased by dupilumab. ( A ) Serum IL-36β levels in AD patients ( n = 36) and healthy control ( n = 15). ( B ) Serum IL-36β levels in severe AD patients ( n = 16) and mild/moderate AD patients ( n = 20). ( C ) Serum IL-36β levels in AD patients ( n = 7) before and after dupilumab treatment. The measured values from individual patients are plotted by dots. Bars represent the median. * p < 0.05.

Article Snippet: Simultaneously, the recombinant human IL-36β protein (R&D systems, Minneapolis, MN, USA) were added, and the cells were incubated at 37 °C and 5% CO 2 .

Techniques:

Journal: International Journal of Molecular Sciences

Article Title: Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis

doi: 10.3390/ijms241311104

Figure Lengend Snippet: IL-36β promotes vascular endothelial growth factor (VEGF)-A and placental growth factor (PlGF) mRNA expression in HaCaT cells. ( A , B ) HaCaT were cultured with recombinant IL-36β (0, 100 ng/mL) for 24 h. Messenger RNA levels of the indicated Th2 cytokines and chemokines ( A ) and angiogenic factors ( B ) were determined by quantitative RT-PCR. One representative result from three independent experiments. The measured values from individual samples are plotted by dots. Bars represent the median. ( n = 4–6). * p < 0.05.

Article Snippet: Simultaneously, the recombinant human IL-36β protein (R&D systems, Minneapolis, MN, USA) were added, and the cells were incubated at 37 °C and 5% CO 2 .

Techniques: Expressing, Cell Culture, Recombinant, Quantitative RT-PCR

Journal: International Journal of Molecular Sciences

Article Title: Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis

doi: 10.3390/ijms241311104

Figure Lengend Snippet: IL-36β enhances vascular endothelial growth factor (VEGF)-A protein production via extracellular signal-regulated kinase (ERK)-1/2 pathway from HaCaT cells. ( A ) HaCaT cells were cultured with recombinant IL-36β (0, 50, 100 ng/mL) for 24 h. Supernatant IL-36β levels were evaluated by enzyme-linked immunosorbent assay. ( B ) HaCaT cells were cultured with recombinant IL-36β (100 ng/mL) for 24 h in the absence or after preincubation with U0126 (20 nM), LY294002 (20 nM), SB203580 (20 nM), or sc-514 (40 nM). Supernatant IL-36β levels were evaluated by enzyme-linked immunosorbent assay. One representative result from three independent experiments. The measured values from individual samples are plotted by dots. Bars represent the median. ( n = 6). * p < 0.05. ** p < 0.01.

Article Snippet: Simultaneously, the recombinant human IL-36β protein (R&D systems, Minneapolis, MN, USA) were added, and the cells were incubated at 37 °C and 5% CO 2 .

Techniques: Cell Culture, Recombinant, Enzyme-linked Immunosorbent Assay

Journal: International Journal of Molecular Sciences

Article Title: Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis

doi: 10.3390/ijms241311104

Figure Lengend Snippet: IL-36β staining intensity in epidermal keratinocytes is correlated with the number of dermal vessels in lesional skin with atopic dermatitis (AD). ( A – D ) Vascular endothelial growth factor (VEGF)-A ( A , B ) and plancental growth factor (PlGF) ( C , D ) staining in healthy skin and AD lesional skin ( n = 10, respectively). Representative images of VEGF-A and PlGF staining in AD skin ( A , C ), and in healthy skin ( B , D ) are shown (original magnification ×400). Arrows point to representative keratinocytes with the nuclear staining. ( E , F ) Double staining of IL-36β (red) and CD34 (brown) in AD lesional skin ( n = 10). Representative images of AD skin with relatively few dermal vessels ( E ) and with relatively abundant dermal vessels ( F ) are shown (original magnification ×200). ( G ) The correlation between IL-36β staining intensity and the number of CD34-positive dermal vessels ( n = 10). The measured values from individual patients are plotted by dots.

Article Snippet: Simultaneously, the recombinant human IL-36β protein (R&D systems, Minneapolis, MN, USA) were added, and the cells were incubated at 37 °C and 5% CO 2 .

Techniques: Staining, Double Staining

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

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

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

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

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

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

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

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

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

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

Journal: mAbs

Article Title: Generation and characterization of ABT-981, a dual variable domain immunoglobulin (DVD-Ig TM ) molecule that specifically and potently neutralizes both IL-1α and IL-1β

doi: 10.1080/19420862.2015.1026501

Figure Lengend Snippet: Specificity of ABT-981 to human IL-1α and IL-1β

Article Snippet: Recombinant human proteins were provided by the following sources: IL-1α (AbbVie), IL-1β (AbbVie), IL-1ra/IL-1F3, (R&D Systems, 280-RA-050), IL-18/IL-1F4 (AbbVie), IL-36Ra/IL-1F5 (R&D Systems, 1275-IL-025), IL-36α/IL-1F6 (R&D Systems 1078-IL-025), FIL1ζ /IL-1F7 (R&D Systems, 1975-IL-025), IL-36β/IL-1F8 (R&D Systems, 1099-IL-025), IL-36γ/IL-1F9 (R&D Systems, 2320-IL-025), IL-1F10 (Origene, TP313987).

Techniques: Binding Assay