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recombinant mouse il 36γ il1f9 protein (R&D Systems)

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R&D Systems recombinant mouse il 36γ il1f9 protein
Recombinant Mouse Il 36γ Il1f9 Protein, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/recombinant+mouse+il+36%CE%B3+il+1f9+protein/pm38838402-113-1-8?v=R%26D+Systems
Average 92 stars, based on 6 article reviews

recombinant mouse il 36γ il1f9 protein - by Bioz Stars, 2026-08

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IL-36γ is causative for the liver injury in RVFV cl13-infected IFNAR -/- mice. C57BL/6 (WT) and IFNAR -/- mice were i.p. infected with 2x10 4 pfu/200 µl RVFV cl13. (A) IL-36γ was measured 30 hpi within the serum using an ELISA method (n=4-6). (B) C57BL/6 (WT) mice were i.v. injected with 1 µg recombinant IL-36γ. ALT activity within the serum was measured 3 hours post treatment (n=3). (C) RVFV cl13-infected IFNAR -/- mice were i.v injected with 6 µg rIL-36RA in 200 µl 12 and 24 hpi. RVFV cl13-infected IFNAR -/- mice served as control. ALT activity was measured 30 hpi (n=5). (D) Histological analyses were performed using H&E staining. Liver sections of RVFV cl13-infected WT and IFNAR -/- mice were prepared 30 hpi as described earlier . Additionally, RVFV cl13-infected IFNAR -/- mice were rIL-36RA-treated (all n=2). Untreated animals served as controls. Arrows exemplarily indicate apoptotic bodies within the tissue. (E) Organs of WT and IFNAR -/- mice were harvested 30 hours post RVFV infection and analyzed for the viral load by plaque assay (n=2-6). Error bars indicate standard deviations. * < 0.05; ** < 0.01 (Welch’s t-test).

Journal: Frontiers in Immunology

Article Title: Interleukin-36γ is causative for liver damage upon infection with Rift Valley fever virus in type I interferon receptor-deficient mice

doi: 10.3389/fimmu.2023.1194733

Figure Lengend Snippet: IL-36γ is causative for the liver injury in RVFV cl13-infected IFNAR -/- mice. C57BL/6 (WT) and IFNAR -/- mice were i.p. infected with 2x10 4 pfu/200 µl RVFV cl13. (A) IL-36γ was measured 30 hpi within the serum using an ELISA method (n=4-6). (B) C57BL/6 (WT) mice were i.v. injected with 1 µg recombinant IL-36γ. ALT activity within the serum was measured 3 hours post treatment (n=3). (C) RVFV cl13-infected IFNAR -/- mice were i.v injected with 6 µg rIL-36RA in 200 µl 12 and 24 hpi. RVFV cl13-infected IFNAR -/- mice served as control. ALT activity was measured 30 hpi (n=5). (D) Histological analyses were performed using H&E staining. Liver sections of RVFV cl13-infected WT and IFNAR -/- mice were prepared 30 hpi as described earlier . Additionally, RVFV cl13-infected IFNAR -/- mice were rIL-36RA-treated (all n=2). Untreated animals served as controls. Arrows exemplarily indicate apoptotic bodies within the tissue. (E) Organs of WT and IFNAR -/- mice were harvested 30 hours post RVFV infection and analyzed for the viral load by plaque assay (n=2-6). Error bars indicate standard deviations. * < 0.05; ** < 0.01 (Welch’s t-test).

Article Snippet: Recombinant mouse IL-36γ/IL-1F9 (aa 13-164; R&D) was diluted in PBS and intravenously (i.v.) injected (1 μg in a volume of 200 μl).

Techniques: Infection, Enzyme-linked Immunosorbent Assay, Injection, Recombinant, Activity Assay, Control, Staining, Plaque Assay

PEC are the main source of IL-36γ upon RVFV cl13 infection of IFNAR -/- mice. (A) To exclude genotype-specific differences in basal expression levels, spleen, liver, and peritoneal exudate cells (PEC) of C57BL/6 (WT) and IFNAR -/- mice (each n=4) were isolated and RNA was prepared as described elsewhere . Expression of IL-36γ was determined by qRT-PCR analyses. All values were normalized to WT animals; n.s.=not significant (Mann Whitney test). (B) C57BL/6 (WT) and IFNAR -/- mice (n=4-9) were i.p. infected with 2x10 4 pfu RVFV cl13 in 200 µl. Spleen, liver, and PEC were isolated 24 hpi infection and RNA was prepared as described earlier . Expression of IL-36γ was determined by qRT-PCR analyses. (C) ISRE-eGFP mice were either left untreated or infected with RVFV cl13 for 30 hours. PEC were isolated and analyzed for eGFP expression by flow cytometry. eGFP-positive cells were further characterized as CD11b + F4/80 + (one representative staining out of three is shown). Error bars indicate standard deviations; * < 0.05 (Welch’s t-test); n.s., not significant.

Journal: Frontiers in Immunology

Article Title: Interleukin-36γ is causative for liver damage upon infection with Rift Valley fever virus in type I interferon receptor-deficient mice

doi: 10.3389/fimmu.2023.1194733

Figure Lengend Snippet: PEC are the main source of IL-36γ upon RVFV cl13 infection of IFNAR -/- mice. (A) To exclude genotype-specific differences in basal expression levels, spleen, liver, and peritoneal exudate cells (PEC) of C57BL/6 (WT) and IFNAR -/- mice (each n=4) were isolated and RNA was prepared as described elsewhere . Expression of IL-36γ was determined by qRT-PCR analyses. All values were normalized to WT animals; n.s.=not significant (Mann Whitney test). (B) C57BL/6 (WT) and IFNAR -/- mice (n=4-9) were i.p. infected with 2x10 4 pfu RVFV cl13 in 200 µl. Spleen, liver, and PEC were isolated 24 hpi infection and RNA was prepared as described earlier . Expression of IL-36γ was determined by qRT-PCR analyses. (C) ISRE-eGFP mice were either left untreated or infected with RVFV cl13 for 30 hours. PEC were isolated and analyzed for eGFP expression by flow cytometry. eGFP-positive cells were further characterized as CD11b + F4/80 + (one representative staining out of three is shown). Error bars indicate standard deviations; * < 0.05 (Welch’s t-test); n.s., not significant.

Article Snippet: Recombinant mouse IL-36γ/IL-1F9 (aa 13-164; R&D) was diluted in PBS and intravenously (i.v.) injected (1 μg in a volume of 200 μl).

Techniques: Infection, Expressing, Isolation, Quantitative RT-PCR, MANN-WHITNEY, Flow Cytometry, Staining

Myeloid cells need to sense type I IFN in order to protect from IL-36γ-mediated liver injury. IFNAR -/- , Mye-IFNAR -/- , DC-IFNAR -/- , and T-IFNAR -/- mice were i.p. infected with 2x10 4 pfu RVFV cl13 in 200 µl. (A) ALT activity was measured 0 and 30 hpi infection (n=3-4). (B) Induction of IL-36γ within the PEC was determined by qRT-PCR analyses (n=5-8); * < 0.05; ** < 0.01 (Welch’s t-test); n.s., not significant.

Journal: Frontiers in Immunology

Article Title: Interleukin-36γ is causative for liver damage upon infection with Rift Valley fever virus in type I interferon receptor-deficient mice

doi: 10.3389/fimmu.2023.1194733

Figure Lengend Snippet: Myeloid cells need to sense type I IFN in order to protect from IL-36γ-mediated liver injury. IFNAR -/- , Mye-IFNAR -/- , DC-IFNAR -/- , and T-IFNAR -/- mice were i.p. infected with 2x10 4 pfu RVFV cl13 in 200 µl. (A) ALT activity was measured 0 and 30 hpi infection (n=3-4). (B) Induction of IL-36γ within the PEC was determined by qRT-PCR analyses (n=5-8); * < 0.05; ** < 0.01 (Welch’s t-test); n.s., not significant.

Article Snippet: Recombinant mouse IL-36γ/IL-1F9 (aa 13-164; R&D) was diluted in PBS and intravenously (i.v.) injected (1 μg in a volume of 200 μl).

Techniques: Infection, Activity Assay, Quantitative RT-PCR

MAVS is critically involved in IL-36γ induction and IL-36γ-mediated liver injury upon RVFV cl13 infection of IFNAR -/- mice. IFNAR -/- , MAVS -/- IFNAR -/- , and MyD88 -/- IFNAR -/- mice were i.p. infected with 2x10 4 pfu RVFV cl13 in 200 µl for 30 hours. (A) IL-36γ induction was investigated by qRT-PCR analyses of the PEC (n=4-6). (B) ALT activity was measured in serum samples at 30 hours post infection (n=4-8). (C) Viral load in different organs was analyzed by plaque assay (n=4-7). Error bars indicate standard deviations; * < 0.05; ** < 0.01; n.s., not significant.

Journal: Frontiers in Immunology

Article Title: Interleukin-36γ is causative for liver damage upon infection with Rift Valley fever virus in type I interferon receptor-deficient mice

doi: 10.3389/fimmu.2023.1194733

Figure Lengend Snippet: MAVS is critically involved in IL-36γ induction and IL-36γ-mediated liver injury upon RVFV cl13 infection of IFNAR -/- mice. IFNAR -/- , MAVS -/- IFNAR -/- , and MyD88 -/- IFNAR -/- mice were i.p. infected with 2x10 4 pfu RVFV cl13 in 200 µl for 30 hours. (A) IL-36γ induction was investigated by qRT-PCR analyses of the PEC (n=4-6). (B) ALT activity was measured in serum samples at 30 hours post infection (n=4-8). (C) Viral load in different organs was analyzed by plaque assay (n=4-7). Error bars indicate standard deviations; * < 0.05; ** < 0.01; n.s., not significant.

Article Snippet: Recombinant mouse IL-36γ/IL-1F9 (aa 13-164; R&D) was diluted in PBS and intravenously (i.v.) injected (1 μg in a volume of 200 μl).

Techniques: Infection, Quantitative RT-PCR, Activity Assay, Plaque Assay

a Neutrophil and macrophage counts and myeloperoxidase concentration in the bronchoalveolar lavage fluid (BALF) from room air (RA) exposed (WT n = 9; Il36r −/− n = 6) and 3-week cigarette smoke (CS) exposed mice (WT n = 10; Il36r −/− n = 10). b – d Neutrophil and macrophage counts, CXCL1, IL-1α, IL-1β, and GM-CSF protein concentrations in BALF from untreated ( n = 6) and IL-36γ-exposed mice (intratracheal instillation) ( n = 7). e , f Cxcl1 , Il1a , Il1b , and Il36g mRNA expression in either e naive mouse alveolar macrophages (pooled n = 15 mice) and stimulated in vitro with no cytokines (−), IL-36γ, or IL-1α/IL-1β or f in mouse bone marrow-derived neutrophils (from n = 4 mice) in vitro stimulated with no cytokines (−), IL-36γ, GM-CSF, or IL-36γ+GM-CSF. g Il36r and Il1r mRNA expression in mouse bone marrow-derived neutrophils (from n = 4 mice) in vitro stimulated with no cytokines (−), IL-36γ, GM-CSF, and IL-36γ+GM-CSF. a , e , f * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs all other groups by one-way ANOVA and Tukey’s correction. b , c , d , g ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs untreated by t test. e AMs were pooled from 15 mice, data are presented as (mean ± SEM) of technical triplicates.

Journal: Communications Biology

Article Title: IL36 is a critical upstream amplifier of neutrophilic lung inflammation in mice

doi: 10.1038/s42003-021-01703-3

Figure Lengend Snippet: a Neutrophil and macrophage counts and myeloperoxidase concentration in the bronchoalveolar lavage fluid (BALF) from room air (RA) exposed (WT n = 9; Il36r −/− n = 6) and 3-week cigarette smoke (CS) exposed mice (WT n = 10; Il36r −/− n = 10). b – d Neutrophil and macrophage counts, CXCL1, IL-1α, IL-1β, and GM-CSF protein concentrations in BALF from untreated ( n = 6) and IL-36γ-exposed mice (intratracheal instillation) ( n = 7). e , f Cxcl1 , Il1a , Il1b , and Il36g mRNA expression in either e naive mouse alveolar macrophages (pooled n = 15 mice) and stimulated in vitro with no cytokines (−), IL-36γ, or IL-1α/IL-1β or f in mouse bone marrow-derived neutrophils (from n = 4 mice) in vitro stimulated with no cytokines (−), IL-36γ, GM-CSF, or IL-36γ+GM-CSF. g Il36r and Il1r mRNA expression in mouse bone marrow-derived neutrophils (from n = 4 mice) in vitro stimulated with no cytokines (−), IL-36γ, GM-CSF, and IL-36γ+GM-CSF. a , e , f * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs all other groups by one-way ANOVA and Tukey’s correction. b , c , d , g ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs untreated by t test. e AMs were pooled from 15 mice, data are presented as (mean ± SEM) of technical triplicates.

Article Snippet: For i.t. administration of IL-36γ, female Balb/c mice were anesthetized with isoflurane for 3 min and 1 μg IL-36γ (6996-IL/CF, Lot DAQQ041703A, R&D) that was diluted in PBS in a total volume of 50 μL/animal was administered with a 1-mL syringe during inspiration.

Techniques: Concentration Assay, Expressing, In Vitro, Derivative Assay

a , b CXCL1 , IL1A , IL1B , and IL36G mRNA expression in human peripheral blood-derived neutrophils (from n = 4 donors) in vitro stimulated with no cytokines (−), IL-36γ, GM-CSF, or IL-36γ+GM-CSF. b IL36R and IL1R mRNA expression in human peripheral blood-derived neutrophils (from n = 4 donors) neutrophils in vitro stimulated with no cytokines (−), IL-36γ, GM-CSF, and IL-36γ+GM-CSF. c , d CXCL1, GM-CSF, and IL1α protein concentrations and CXCL1 , IL36G , GM-CSF , IL1A , and IL1B mRNA expression in small airway epithelial cells (SAEC) stimulated with either (−) or IL-36αβγ. a , b * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, vs all other groups by one-way ANOVA and Tukey’s correction. c , d * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs untreated by t test.

Journal: Communications Biology

Article Title: IL36 is a critical upstream amplifier of neutrophilic lung inflammation in mice

doi: 10.1038/s42003-021-01703-3

Figure Lengend Snippet: a , b CXCL1 , IL1A , IL1B , and IL36G mRNA expression in human peripheral blood-derived neutrophils (from n = 4 donors) in vitro stimulated with no cytokines (−), IL-36γ, GM-CSF, or IL-36γ+GM-CSF. b IL36R and IL1R mRNA expression in human peripheral blood-derived neutrophils (from n = 4 donors) neutrophils in vitro stimulated with no cytokines (−), IL-36γ, GM-CSF, and IL-36γ+GM-CSF. c , d CXCL1, GM-CSF, and IL1α protein concentrations and CXCL1 , IL36G , GM-CSF , IL1A , and IL1B mRNA expression in small airway epithelial cells (SAEC) stimulated with either (−) or IL-36αβγ. a , b * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, vs all other groups by one-way ANOVA and Tukey’s correction. c , d * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs untreated by t test.

Techniques: Expressing, Derivative Assay, In Vitro

a Relative mRNA amounts of Il36r in naive mouse bone marrow-derived macrophages (BMDMs, n = 6) in response to no stimulation (−) or stimulation with GM-CSF and IL-36γ. b CXCL1 protein concentrations in supernatant of BMDMs ( n = 4) after no stimulation (−), or stimulation with IL-36αβγ. IL-1α, IL-1β alone, or in combination with GM-CSF and TGFβ c , d Relative mRNA amounts of Il36g , Cxcl1 , Il1a , Il1b , Il1r1 , Il1rn , and Il36rn in BMDMs ( n = 4) ( c ) and primary mouse fibroblasts ( n = 4) ( d ) after no stimulation (−) or stimulation with IL-36αβγ, IL-1α, IL-1β alone, or in combination with GM-CSF and TGF-β. e Relative mRNA amounts in primary mouse fibroblasts ( n = 4) of Il36r after no stimulation (−) or stimulation with IL-36αβγ or GM-CSF and TGF-β. Shown are the mean values ± SEM of biological replicates. a – d * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs all other groups by one-way ANOVA and Tukey’s correction. e * P ≤ 0.05, vs untreated by t test.

Journal: Communications Biology

Article Title: IL36 is a critical upstream amplifier of neutrophilic lung inflammation in mice

doi: 10.1038/s42003-021-01703-3

Figure Lengend Snippet: a Relative mRNA amounts of Il36r in naive mouse bone marrow-derived macrophages (BMDMs, n = 6) in response to no stimulation (−) or stimulation with GM-CSF and IL-36γ. b CXCL1 protein concentrations in supernatant of BMDMs ( n = 4) after no stimulation (−), or stimulation with IL-36αβγ. IL-1α, IL-1β alone, or in combination with GM-CSF and TGFβ c , d Relative mRNA amounts of Il36g , Cxcl1 , Il1a , Il1b , Il1r1 , Il1rn , and Il36rn in BMDMs ( n = 4) ( c ) and primary mouse fibroblasts ( n = 4) ( d ) after no stimulation (−) or stimulation with IL-36αβγ, IL-1α, IL-1β alone, or in combination with GM-CSF and TGF-β. e Relative mRNA amounts in primary mouse fibroblasts ( n = 4) of Il36r after no stimulation (−) or stimulation with IL-36αβγ or GM-CSF and TGF-β. Shown are the mean values ± SEM of biological replicates. a – d * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs all other groups by one-way ANOVA and Tukey’s correction. e * P ≤ 0.05, vs untreated by t test.

Techniques: Derivative Assay

a Relative mRNA amounts in human monocyte-derived macrophages (MDM) (depicted are mean values ± SME of technical triplicates from one representative of four experiments) of IL-36G , IL-36R , IL1A , and IL1B and b IL-36γ , IL-36R , IL1A , IL1B , GMCSF , and CXCL1 in primary human lung fibroblasts ( n = 4) after no stimulation (−) or stimulation with IL-36αβγ, GM-CSF alone, or with the combination of IL-36αβγ and GM-CSF. Shown are the mean values ± SEM of biological replicates. a , b * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs all other groups by one-way ANOVA and Tukey’s correction.

Journal: Communications Biology

Article Title: IL36 is a critical upstream amplifier of neutrophilic lung inflammation in mice

doi: 10.1038/s42003-021-01703-3

Figure Lengend Snippet: a Relative mRNA amounts in human monocyte-derived macrophages (MDM) (depicted are mean values ± SME of technical triplicates from one representative of four experiments) of IL-36G , IL-36R , IL1A , and IL1B and b IL-36γ , IL-36R , IL1A , IL1B , GMCSF , and CXCL1 in primary human lung fibroblasts ( n = 4) after no stimulation (−) or stimulation with IL-36αβγ, GM-CSF alone, or with the combination of IL-36αβγ and GM-CSF. Shown are the mean values ± SEM of biological replicates. a , b * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs all other groups by one-way ANOVA and Tukey’s correction.

Techniques: Derivative Assay

a GM-CSF, CXCL1, IL-36γ, IL-1β, and IL-1α protein concentrations and GM-CSF , CXCL1 , IL36G , IL1A , and IL1B mRNA expression of lung epithelial basal cells from healthy donor stimulated with poly(I:C) and LPS (depicted are mean values ± SEM of technical triplicates from one representative of three experiments). * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs all other groups by one-way ANOVA and Tukey’s correction.

Journal: Communications Biology

Article Title: IL36 is a critical upstream amplifier of neutrophilic lung inflammation in mice

doi: 10.1038/s42003-021-01703-3

Figure Lengend Snippet: a GM-CSF, CXCL1, IL-36γ, IL-1β, and IL-1α protein concentrations and GM-CSF , CXCL1 , IL36G , IL1A , and IL1B mRNA expression of lung epithelial basal cells from healthy donor stimulated with poly(I:C) and LPS (depicted are mean values ± SEM of technical triplicates from one representative of three experiments). * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 vs all other groups by one-way ANOVA and Tukey’s correction.

Techniques: Expressing

1 Chronic (e.g., cigarette smoke) or acute (H1N1 or poly(I:C) injury to the lung epithelium promotes release of CXCL1 and GMCSF. 2 CXCL1 promotes neutrophil recruitment while GM-CSF upregulates the IL-36R and IL1RN by neutrophils and promotes IL-36γ expression. 3 IL-36γ activates neutrophils to generate IL1 and IL36. 4 IL-36γ subsequently activates alveolar and interstitial macrophages and fibroblasts to generate IL-1, CXCL1, GM-CSF, MMPs, and more IL-36. GM-CSF also upregulates the lL36R on macrophages and on fibroblasts and sensitizes cells to IL-36. 5 Poly(I:C) as a TLR agonist cooperates with IL-36γ in amplifying activation of macrophages and fibroblasts. Note that IL-36RN is not induced while IL1RN is induced, shifting the balance toward heightened responsiveness to IL-36.

Journal: Communications Biology

Article Title: IL36 is a critical upstream amplifier of neutrophilic lung inflammation in mice

doi: 10.1038/s42003-021-01703-3

Figure Lengend Snippet: 1 Chronic (e.g., cigarette smoke) or acute (H1N1 or poly(I:C) injury to the lung epithelium promotes release of CXCL1 and GMCSF. 2 CXCL1 promotes neutrophil recruitment while GM-CSF upregulates the IL-36R and IL1RN by neutrophils and promotes IL-36γ expression. 3 IL-36γ activates neutrophils to generate IL1 and IL36. 4 IL-36γ subsequently activates alveolar and interstitial macrophages and fibroblasts to generate IL-1, CXCL1, GM-CSF, MMPs, and more IL-36. GM-CSF also upregulates the lL36R on macrophages and on fibroblasts and sensitizes cells to IL-36. 5 Poly(I:C) as a TLR agonist cooperates with IL-36γ in amplifying activation of macrophages and fibroblasts. Note that IL-36RN is not induced while IL1RN is induced, shifting the balance toward heightened responsiveness to IL-36.

Techniques: Expressing, Activation Assay

Journal: Communications Biology

Article Title: IL36 is a critical upstream amplifier of neutrophilic lung inflammation in mice

doi: 10.1038/s42003-021-01703-3

Figure Lengend Snippet: Cytokines used in this study.

Techniques: Concentration Assay

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