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Figure 1. <t>IL-17E</t> promotes skin inﬂammation and favors the preferential recruitment of neutrophils in vivo. Balb/c mice were intradermally injected with recombinant mouse IL-17E or saline in the back for 2 consecutive days. Skin samples were harvested on day 3. (a) Representative hematoxylin and eosin staining of skin from mice treated with IL-17E or saline (n ¼ 8). Original magniﬁcation 10. Scale bar ¼ 50 mm. (b) Proﬁling of the cellular inﬁltrate in the skin of saline- (black bars) and IL-17Eeinjected (red bars) mice by ﬂow cytometry. Cumulative data from three independent experiments (n ¼ 8) are presented as absolute counts per cm2. (c) Representative ﬂow cytometry plots of the experiment shown in b. Full-thickness line gates depict cell populations modiﬁed by IL- 17E treatment. Pseudocolor scale indicates absolute counts, and numbers in the gates refer to frequency relative to CD45þ cells. (d) Immunoﬂuorescence analysis of skin sections stained for DAPI (blue), Ki67 (green), and cytokeratin 10 (red). Original magniﬁcation 40. Scale bar ¼ 20 mm. One representative result is shown (n ¼ 5). White arrows depict Ki-67 positive cells (left panel). Quantitative analysis of Ki67þ cells in the basal layer (n ¼ 5, right panel). (e) Quantitative analysis of the epidermal thickness based on hematoxylin and eosin-stained sections (n ¼ 5). (f) Gene expression analysis was performed using NanoString (Seattle, WA) technology in the skin of mice injected with IL-17E or saline for 3 hours. Volcano plot (left panel) displays differentially expressed genes upon IL-17E treatment. The y-axis corresponds to the mean expression value of log10 P-value, and the x-axis displays the log2 fold change value. The red dots represent the differentially expressed transcripts (threshold > 2 fold change). Heatmap (right panel) of differentially expressed mRNAs in IL-17Eeinjected versus saline (control) group (n ¼ 5). Expression values are colored based on their z-score after normalization across treatments.

Mouse Antihuman Il 17e Mab, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "IL-17E (IL-25) Enhances Innate Immune Responses during Skin Inflammation."

Article Title: IL-17E (IL-25) Enhances Innate Immune Responses during Skin Inflammation.

Journal: The Journal of investigative dermatology

doi: 10.1016/j.jid.2019.01.021

Figure 1. IL-17E promotes skin inﬂammation and favors the preferential recruitment of neutrophils in vivo. Balb/c mice were intradermally injected with recombinant mouse IL-17E or saline in the back for 2 consecutive days. Skin samples were harvested on day 3. (a) Representative hematoxylin and eosin staining of skin from mice treated with IL-17E or saline (n ¼ 8). Original magniﬁcation 10. Scale bar ¼ 50 mm. (b) Proﬁling of the cellular inﬁltrate in the skin of saline- (black bars) and IL-17Eeinjected (red bars) mice by ﬂow cytometry. Cumulative data from three independent experiments (n ¼ 8) are presented as absolute counts per cm2. (c) Representative ﬂow cytometry plots of the experiment shown in b. Full-thickness line gates depict cell populations modiﬁed by IL- 17E treatment. Pseudocolor scale indicates absolute counts, and numbers in the gates refer to frequency relative to CD45þ cells. (d) Immunoﬂuorescence analysis of skin sections stained for DAPI (blue), Ki67 (green), and cytokeratin 10 (red). Original magniﬁcation 40. Scale bar ¼ 20 mm. One representative result is shown (n ¼ 5). White arrows depict Ki-67 positive cells (left panel). Quantitative analysis of Ki67þ cells in the basal layer (n ¼ 5, right panel). (e) Quantitative analysis of the epidermal thickness based on hematoxylin and eosin-stained sections (n ¼ 5). (f) Gene expression analysis was performed using NanoString (Seattle, WA) technology in the skin of mice injected with IL-17E or saline for 3 hours. Volcano plot (left panel) displays differentially expressed genes upon IL-17E treatment. The y-axis corresponds to the mean expression value of log10 P-value, and the x-axis displays the log2 fold change value. The red dots represent the differentially expressed transcripts (threshold > 2 fold change). Heatmap (right panel) of differentially expressed mRNAs in IL-17Eeinjected versus saline (control) group (n ¼ 5). Expression values are colored based on their z-score after normalization across treatments.

Figure Legend Snippet: Figure 1. IL-17E promotes skin inﬂammation and favors the preferential recruitment of neutrophils in vivo. Balb/c mice were intradermally injected with recombinant mouse IL-17E or saline in the back for 2 consecutive days. Skin samples were harvested on day 3. (a) Representative hematoxylin and eosin staining of skin from mice treated with IL-17E or saline (n ¼ 8). Original magniﬁcation 10. Scale bar ¼ 50 mm. (b) Proﬁling of the cellular inﬁltrate in the skin of saline- (black bars) and IL-17Eeinjected (red bars) mice by ﬂow cytometry. Cumulative data from three independent experiments (n ¼ 8) are presented as absolute counts per cm2. (c) Representative ﬂow cytometry plots of the experiment shown in b. Full-thickness line gates depict cell populations modiﬁed by IL- 17E treatment. Pseudocolor scale indicates absolute counts, and numbers in the gates refer to frequency relative to CD45þ cells. (d) Immunoﬂuorescence analysis of skin sections stained for DAPI (blue), Ki67 (green), and cytokeratin 10 (red). Original magniﬁcation 40. Scale bar ¼ 20 mm. One representative result is shown (n ¼ 5). White arrows depict Ki-67 positive cells (left panel). Quantitative analysis of Ki67þ cells in the basal layer (n ¼ 5, right panel). (e) Quantitative analysis of the epidermal thickness based on hematoxylin and eosin-stained sections (n ¼ 5). (f) Gene expression analysis was performed using NanoString (Seattle, WA) technology in the skin of mice injected with IL-17E or saline for 3 hours. Volcano plot (left panel) displays differentially expressed genes upon IL-17E treatment. The y-axis corresponds to the mean expression value of log10 P-value, and the x-axis displays the log2 fold change value. The red dots represent the differentially expressed transcripts (threshold > 2 fold change). Heatmap (right panel) of differentially expressed mRNAs in IL-17Eeinjected versus saline (control) group (n ¼ 5). Expression values are colored based on their z-score after normalization across treatments.

Techniques Used: In Vivo, Injection, Recombinant, Saline, Staining, Cytometry, Gene Expression, Expressing, Control

Figure 3. IL-17E neutralization through blocking antibodies ameliorates imiquimod-induced skin inﬂammation. Wild-type balb/c mice were treated with imiquimod for 3 consecutive days on the shaved back skin and one ear. Next, 100 mg of neutralizing IL-17E antibody or isotype control were injected intraperitoneally1 day before the ﬁrst application and 1 hour before every application. Skin and ear tissue samples were harvested on day 4. (a) Daily body weight variation and percentage of increase in ear swelling expressed as mean standard error of the mean (n ¼ 5). (b) Representative hematoxylin and eosin staining of the back skin and quantitative analysis of the epidermal thickness of imiquimod-treated mice injected with anti-IL-17E (n ¼ 11) or isotype control

Figure Legend Snippet: Figure 3. IL-17E neutralization through blocking antibodies ameliorates imiquimod-induced skin inﬂammation. Wild-type balb/c mice were treated with imiquimod for 3 consecutive days on the shaved back skin and one ear. Next, 100 mg of neutralizing IL-17E antibody or isotype control were injected intraperitoneally1 day before the ﬁrst application and 1 hour before every application. Skin and ear tissue samples were harvested on day 4. (a) Daily body weight variation and percentage of increase in ear swelling expressed as mean standard error of the mean (n ¼ 5). (b) Representative hematoxylin and eosin staining of the back skin and quantitative analysis of the epidermal thickness of imiquimod-treated mice injected with anti-IL-17E (n ¼ 11) or isotype control

Techniques Used: Neutralization, Blocking Assay, Control, Injection, Staining

Figure 4. IL-17E neutralization affects innate immune cell inﬁltration during imiquimod-induced skin inﬂammation. Experimental condition, as in Figure 4. (a) Visualized t-SNE map of cells isolated from the skin of mice treated with imiquimod. Clusters (cell populations) were identiﬁed by manual gating. One representative result of each group is shown (n ¼ 10 for isotype control group; n ¼ 11 for a-IL-17E-treated group). (b) Based on clusters identiﬁed in a, median intensities for each marker were calculated and plotted as a heatmap. (c, d) Histogram showing the mean ﬂuorescence intensity of the indicated markers in each cell cluster (c) belonging to the NK population (clusters 1e3) or (d) belonging to the neutrophil population (clusters 10 to 13) in the anti-IL-17E treated group. max, maximum; NK, natural killer; t-SNE, t-distributed stochastic neighbor embedding.

Figure Legend Snippet: Figure 4. IL-17E neutralization affects innate immune cell inﬁltration during imiquimod-induced skin inﬂammation. Experimental condition, as in Figure 4. (a) Visualized t-SNE map of cells isolated from the skin of mice treated with imiquimod. Clusters (cell populations) were identiﬁed by manual gating. One representative result of each group is shown (n ¼ 10 for isotype control group; n ¼ 11 for a-IL-17E-treated group). (b) Based on clusters identiﬁed in a, median intensities for each marker were calculated and plotted as a heatmap. (c, d) Histogram showing the mean ﬂuorescence intensity of the indicated markers in each cell cluster (c) belonging to the NK population (clusters 1e3) or (d) belonging to the neutrophil population (clusters 10 to 13) in the anti-IL-17E treated group. max, maximum; NK, natural killer; t-SNE, t-distributed stochastic neighbor embedding.

Techniques Used: Neutralization, Isolation, Control, Marker

Figure 5. IL-17E promotes the recruitment of human neutrophils via activation of macrophages in a p38-dependent mechanism. (a) mRNA level of human IL-8 (left panel) and murine Cxcl1 and Cxcl2 (right panel) in IL-17Eetreated M2 macrophages from humans and mice, respectively. (b) IL-8 levels as assessed by ELISA in supernatants of primary keratinocytes (n ¼ 4) cultured in the presence of IL-17E or TNF (right panel). (c) mRNA levels assessed by quantitative PCR in M2 polarized macrophages pretreated for 30 minutes with a p38 MAPK (SB202190) or NF-kB inhibitor (JSH 23) and then stimulated with IL-17E for a further 6 hours. mRNA levels relative to the untreated condition are shown as mean standard error of the mean (n 5). (d) Immunoblotting analysis of M2 polarized macrophages stimulated with 100 ng/ml of IL-17E for the indicated time points (n ¼ 5, one representative result is shown). (e) Neutrophil migration induced by IL-8 (50 ng/ml) or IL-17E (100 ng/ml) in a classic Transwell assay (Nunc, Roskilde, Denmark) (left panel). M2 macrophages were left unstimulated (unstim.) or treated with IL-17E in the presence or not of SB202190 for 24 hours. Supernatants were retrieved and used to assess neutrophil migration. IL-8 neutralizing antibodies were added to the conditioned media of macrophages stimulated with IL-17E 30 minutes before assessing chemotaxis. Data from one representative experiment are expressed as relative to control media and presented as the mean standard error of the mean (n ¼ 3). (f) IL-8 protein levels assessed by ELISA in supernatants of M2 polarized macrophages. The protein levels relative to untreated condition are shown as mean standard error of the mean (n 5). Signiﬁcant differences were assessed by Wilcoxon signed rank test. *P ¼ 0.01 to 0.05. Ctrl, control; min, minute; p-, phosphorylated.

Figure Legend Snippet: Figure 5. IL-17E promotes the recruitment of human neutrophils via activation of macrophages in a p38-dependent mechanism. (a) mRNA level of human IL-8 (left panel) and murine Cxcl1 and Cxcl2 (right panel) in IL-17Eetreated M2 macrophages from humans and mice, respectively. (b) IL-8 levels as assessed by ELISA in supernatants of primary keratinocytes (n ¼ 4) cultured in the presence of IL-17E or TNF (right panel). (c) mRNA levels assessed by quantitative PCR in M2 polarized macrophages pretreated for 30 minutes with a p38 MAPK (SB202190) or NF-kB inhibitor (JSH 23) and then stimulated with IL-17E for a further 6 hours. mRNA levels relative to the untreated condition are shown as mean standard error of the mean (n 5). (d) Immunoblotting analysis of M2 polarized macrophages stimulated with 100 ng/ml of IL-17E for the indicated time points (n ¼ 5, one representative result is shown). (e) Neutrophil migration induced by IL-8 (50 ng/ml) or IL-17E (100 ng/ml) in a classic Transwell assay (Nunc, Roskilde, Denmark) (left panel). M2 macrophages were left unstimulated (unstim.) or treated with IL-17E in the presence or not of SB202190 for 24 hours. Supernatants were retrieved and used to assess neutrophil migration. IL-8 neutralizing antibodies were added to the conditioned media of macrophages stimulated with IL-17E 30 minutes before assessing chemotaxis. Data from one representative experiment are expressed as relative to control media and presented as the mean standard error of the mean (n ¼ 3). (f) IL-8 protein levels assessed by ELISA in supernatants of M2 polarized macrophages. The protein levels relative to untreated condition are shown as mean standard error of the mean (n 5). Signiﬁcant differences were assessed by Wilcoxon signed rank test. *P ¼ 0.01 to 0.05. Ctrl, control; min, minute; p-, phosphorylated.

Techniques Used: Activation Assay, Enzyme-linked Immunosorbent Assay, Cell Culture, Real-time Polymerase Chain Reaction, Western Blot, Migration, Transwell Assay, Chemotaxis Assay, Control

Figure 6. An increase in IL-17ED cells may indicate a neutrophil inﬁltration in human skin inﬂammatory conditions. Expression of myeloperoxidase (green) in combination with IL-17E (red) and DAPI (blue) assessed by immunoﬂuorescence in the skin of healthy volunteers (n ¼ 4) and patients with acute generalized exanthematous pustulosis (n ¼ 3) and pyoderma gangrenosum (n ¼ 4). Original magniﬁcation 20. Scale bar ¼ 50 mm. (b) Quantiﬁcation of dermal IL-17Eþ and MPOþ cells in the samples, as in a. (c) Quantiﬁcation of the expression of IL-17E in the epidermis of the samples shown in a. AGEP, acute generalized exanthematous pustulosis; MPO, myeloperoxidase; PG, pyoderma gangrenosum.

Figure Legend Snippet: Figure 6. An increase in IL-17ED cells may indicate a neutrophil inﬁltration in human skin inﬂammatory conditions. Expression of myeloperoxidase (green) in combination with IL-17E (red) and DAPI (blue) assessed by immunoﬂuorescence in the skin of healthy volunteers (n ¼ 4) and patients with acute generalized exanthematous pustulosis (n ¼ 3) and pyoderma gangrenosum (n ¼ 4). Original magniﬁcation 20. Scale bar ¼ 50 mm. (b) Quantiﬁcation of dermal IL-17Eþ and MPOþ cells in the samples, as in a. (c) Quantiﬁcation of the expression of IL-17E in the epidermis of the samples shown in a. AGEP, acute generalized exanthematous pustulosis; MPO, myeloperoxidase; PG, pyoderma gangrenosum.

Techniques Used: Expressing

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Journal: The Journal of investigative dermatology

Article Title: IL-17E (IL-25) Enhances Innate Immune Responses during Skin Inflammation.

doi: 10.1016/j.jid.2019.01.021

Figure Lengend Snippet: Figure 1. IL-17E promotes skin inﬂammation and favors the preferential recruitment of neutrophils in vivo. Balb/c mice were intradermally injected with recombinant mouse IL-17E or saline in the back for 2 consecutive days. Skin samples were harvested on day 3. (a) Representative hematoxylin and eosin staining of skin from mice treated with IL-17E or saline (n ¼ 8). Original magniﬁcation 10. Scale bar ¼ 50 mm. (b) Proﬁling of the cellular inﬁltrate in the skin of saline- (black bars) and IL-17Eeinjected (red bars) mice by ﬂow cytometry. Cumulative data from three independent experiments (n ¼ 8) are presented as absolute counts per cm2. (c) Representative ﬂow cytometry plots of the experiment shown in b. Full-thickness line gates depict cell populations modiﬁed by IL- 17E treatment. Pseudocolor scale indicates absolute counts, and numbers in the gates refer to frequency relative to CD45þ cells. (d) Immunoﬂuorescence analysis of skin sections stained for DAPI (blue), Ki67 (green), and cytokeratin 10 (red). Original magniﬁcation 40. Scale bar ¼ 20 mm. One representative result is shown (n ¼ 5). White arrows depict Ki-67 positive cells (left panel). Quantitative analysis of Ki67þ cells in the basal layer (n ¼ 5, right panel). (e) Quantitative analysis of the epidermal thickness based on hematoxylin and eosin-stained sections (n ¼ 5). (f) Gene expression analysis was performed using NanoString (Seattle, WA) technology in the skin of mice injected with IL-17E or saline for 3 hours. Volcano plot (left panel) displays differentially expressed genes upon IL-17E treatment. The y-axis corresponds to the mean expression value of log10 P-value, and the x-axis displays the log2 fold change value. The red dots represent the differentially expressed transcripts (threshold > 2 fold change). Heatmap (right panel) of differentially expressed mRNAs in IL-17Eeinjected versus saline (control) group (n ¼ 5). Expression values are colored based on their z-score after normalization across treatments.

Article Snippet: Mouse antihuman IL-17E mAb (clone 182293) and polyclonal goat anti-human myeloperoxidase antibody were from R&D Systems, rabbit anti-human cytokeratin 10 was from BioSB (Santa Barbara, CA), and rat anti-mouse Ki67 mAb (clone 16A8) and rat anti-mouse Ly6G (clone 1A8) were from Biolegend.

Techniques: In Vivo, Injection, Recombinant, Saline, Staining, Cytometry, Gene Expression, Expressing, Control

Journal: The Journal of investigative dermatology

Article Title: IL-17E (IL-25) Enhances Innate Immune Responses during Skin Inflammation.

doi: 10.1016/j.jid.2019.01.021

Figure Lengend Snippet: Figure 3. IL-17E neutralization through blocking antibodies ameliorates imiquimod-induced skin inﬂammation. Wild-type balb/c mice were treated with imiquimod for 3 consecutive days on the shaved back skin and one ear. Next, 100 mg of neutralizing IL-17E antibody or isotype control were injected intraperitoneally1 day before the ﬁrst application and 1 hour before every application. Skin and ear tissue samples were harvested on day 4. (a) Daily body weight variation and percentage of increase in ear swelling expressed as mean standard error of the mean (n ¼ 5). (b) Representative hematoxylin and eosin staining of the back skin and quantitative analysis of the epidermal thickness of imiquimod-treated mice injected with anti-IL-17E (n ¼ 11) or isotype control

Techniques: Neutralization, Blocking Assay, Control, Injection, Staining

Journal: The Journal of investigative dermatology

Article Title: IL-17E (IL-25) Enhances Innate Immune Responses during Skin Inflammation.

doi: 10.1016/j.jid.2019.01.021

Figure Lengend Snippet: Figure 4. IL-17E neutralization affects innate immune cell inﬁltration during imiquimod-induced skin inﬂammation. Experimental condition, as in Figure 4. (a) Visualized t-SNE map of cells isolated from the skin of mice treated with imiquimod. Clusters (cell populations) were identiﬁed by manual gating. One representative result of each group is shown (n ¼ 10 for isotype control group; n ¼ 11 for a-IL-17E-treated group). (b) Based on clusters identiﬁed in a, median intensities for each marker were calculated and plotted as a heatmap. (c, d) Histogram showing the mean ﬂuorescence intensity of the indicated markers in each cell cluster (c) belonging to the NK population (clusters 1e3) or (d) belonging to the neutrophil population (clusters 10 to 13) in the anti-IL-17E treated group. max, maximum; NK, natural killer; t-SNE, t-distributed stochastic neighbor embedding.

Techniques: Neutralization, Isolation, Control, Marker

Journal: The Journal of investigative dermatology

Article Title: IL-17E (IL-25) Enhances Innate Immune Responses during Skin Inflammation.

doi: 10.1016/j.jid.2019.01.021

Figure Lengend Snippet: Figure 5. IL-17E promotes the recruitment of human neutrophils via activation of macrophages in a p38-dependent mechanism. (a) mRNA level of human IL-8 (left panel) and murine Cxcl1 and Cxcl2 (right panel) in IL-17Eetreated M2 macrophages from humans and mice, respectively. (b) IL-8 levels as assessed by ELISA in supernatants of primary keratinocytes (n ¼ 4) cultured in the presence of IL-17E or TNF (right panel). (c) mRNA levels assessed by quantitative PCR in M2 polarized macrophages pretreated for 30 minutes with a p38 MAPK (SB202190) or NF-kB inhibitor (JSH 23) and then stimulated with IL-17E for a further 6 hours. mRNA levels relative to the untreated condition are shown as mean standard error of the mean (n 5). (d) Immunoblotting analysis of M2 polarized macrophages stimulated with 100 ng/ml of IL-17E for the indicated time points (n ¼ 5, one representative result is shown). (e) Neutrophil migration induced by IL-8 (50 ng/ml) or IL-17E (100 ng/ml) in a classic Transwell assay (Nunc, Roskilde, Denmark) (left panel). M2 macrophages were left unstimulated (unstim.) or treated with IL-17E in the presence or not of SB202190 for 24 hours. Supernatants were retrieved and used to assess neutrophil migration. IL-8 neutralizing antibodies were added to the conditioned media of macrophages stimulated with IL-17E 30 minutes before assessing chemotaxis. Data from one representative experiment are expressed as relative to control media and presented as the mean standard error of the mean (n ¼ 3). (f) IL-8 protein levels assessed by ELISA in supernatants of M2 polarized macrophages. The protein levels relative to untreated condition are shown as mean standard error of the mean (n 5). Signiﬁcant differences were assessed by Wilcoxon signed rank test. *P ¼ 0.01 to 0.05. Ctrl, control; min, minute; p-, phosphorylated.

Techniques: Activation Assay, Enzyme-linked Immunosorbent Assay, Cell Culture, Real-time Polymerase Chain Reaction, Western Blot, Migration, Transwell Assay, Chemotaxis Assay, Control

Journal: The Journal of investigative dermatology

Article Title: IL-17E (IL-25) Enhances Innate Immune Responses during Skin Inflammation.

doi: 10.1016/j.jid.2019.01.021

Figure Lengend Snippet: Figure 6. An increase in IL-17ED cells may indicate a neutrophil inﬁltration in human skin inﬂammatory conditions. Expression of myeloperoxidase (green) in combination with IL-17E (red) and DAPI (blue) assessed by immunoﬂuorescence in the skin of healthy volunteers (n ¼ 4) and patients with acute generalized exanthematous pustulosis (n ¼ 3) and pyoderma gangrenosum (n ¼ 4). Original magniﬁcation 20. Scale bar ¼ 50 mm. (b) Quantiﬁcation of dermal IL-17Eþ and MPOþ cells in the samples, as in a. (c) Quantiﬁcation of the expression of IL-17E in the epidermis of the samples shown in a. AGEP, acute generalized exanthematous pustulosis; MPO, myeloperoxidase; PG, pyoderma gangrenosum.

Techniques: Expressing

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