il 36r Search Results


90
OriGene human il 36r
Human Il 36r, supplied by OriGene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/il+36r/IL1RL2+(NM_003854)+Human+Tagged+ORF+Clone/pm28379093-302-31-37
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Shanghai GenePharma sirnas targeting human cd93, il-36r, ddxs and sf2
Sirnas Targeting Human Cd93, Il 36r, Ddxs And Sf2, supplied by Shanghai GenePharma, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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CH Instruments il-36r antagonist
The treatments targeting of lymphocytes in vivo .
Il 36r Antagonist, supplied by CH Instruments, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/il+36r/il+36r+antagonist/pmc08488268-302-4-22
Average 90 stars, based on 1 article reviews
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Innovagen AB anti-il-36r_bm2-higg4-a647
The treatments targeting of lymphocytes in vivo .
Anti Il 36r Bm2 Higg4 A647, supplied by Innovagen AB, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/il+36r/anti+il+36r+bm2+higg4+a647/pmc12184588-34-0-7
Average 90 stars, based on 1 article reviews
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86
Boehringer Ingelheim anti il 36r mab
WT and <t>IL-36R</t> −/− mice dorsal skin was naive or e.c. exposed to S. aureus (1 × 10 8 CFU) for 7 days. Photographs and disease score were taken on day 7, and skin biopsies (10 mm), and lungs were harvested on day 10 ( n ≥ 9 per group). (A) Representative skin photographs. (B) Mean disease score (±SEM). (C) Representative lung and bronchiole histology (H&E, scale bars: 1 mm and 100 μm). (D) Lung inflammation (%) ±SEM from lung sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (E) Mean bronchiole epidermal thickness (±SEM). (F) GO biological process enrichment pathway analysis of RNA-seq from day 10 naive and e.c.-exposed (WT) lungs ( n = 5 per group). resp, responses; reg., regulation; pos., positive; leuk., leukocyte; migr., migration; sig., signaling. (G) Mean number of lung PMNs, monocytes, and eosinophils (±SEM) in day 10 lungs as measured by fluorescence-activated cell sorting (FACS). ns, not significant; ** p < 0.01, *** p < 0.001, and **** p < 0.0001 as calculated by a two-tailed Student’s t test (B, D, and E) or one-way ANOVA multiple comparisons test with Tukey correction (G). Results are combined from at least 2 independent experiments. See also .
Anti Il 36r Mab, supplied by Boehringer Ingelheim, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/il+36r/36r+anti+il/pmc12461889-36-0-3
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90
Regeneron inc il-36r–deficient mice
WT and <t>IL-36R</t> −/− mice dorsal skin was naive or e.c. exposed to S. aureus (1 × 10 8 CFU) for 7 days. Photographs and disease score were taken on day 7, and skin biopsies (10 mm), and lungs were harvested on day 10 ( n ≥ 9 per group). (A) Representative skin photographs. (B) Mean disease score (±SEM). (C) Representative lung and bronchiole histology (H&E, scale bars: 1 mm and 100 μm). (D) Lung inflammation (%) ±SEM from lung sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (E) Mean bronchiole epidermal thickness (±SEM). (F) GO biological process enrichment pathway analysis of RNA-seq from day 10 naive and e.c.-exposed (WT) lungs ( n = 5 per group). resp, responses; reg., regulation; pos., positive; leuk., leukocyte; migr., migration; sig., signaling. (G) Mean number of lung PMNs, monocytes, and eosinophils (±SEM) in day 10 lungs as measured by fluorescence-activated cell sorting (FACS). ns, not significant; ** p < 0.01, *** p < 0.001, and **** p < 0.0001 as calculated by a two-tailed Student’s t test (B, D, and E) or one-way ANOVA multiple comparisons test with Tukey correction (G). Results are combined from at least 2 independent experiments. See also .
Il 36r–Deficient Mice, supplied by Regeneron inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/il+36r/il+36r+deficient+mice/pm33443029-153-33-37
Average 90 stars, based on 1 article reviews
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86
Novoprotein rhil 36r agonist
WT and <t>IL-36R</t> −/− mice dorsal skin was naive or e.c. exposed to S. aureus (1 × 10 8 CFU) for 7 days. Photographs and disease score were taken on day 7, and skin biopsies (10 mm), and lungs were harvested on day 10 ( n ≥ 9 per group). (A) Representative skin photographs. (B) Mean disease score (±SEM). (C) Representative lung and bronchiole histology (H&E, scale bars: 1 mm and 100 μm). (D) Lung inflammation (%) ±SEM from lung sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (E) Mean bronchiole epidermal thickness (±SEM). (F) GO biological process enrichment pathway analysis of RNA-seq from day 10 naive and e.c.-exposed (WT) lungs ( n = 5 per group). resp, responses; reg., regulation; pos., positive; leuk., leukocyte; migr., migration; sig., signaling. (G) Mean number of lung PMNs, monocytes, and eosinophils (±SEM) in day 10 lungs as measured by fluorescence-activated cell sorting (FACS). ns, not significant; ** p < 0.01, *** p < 0.001, and **** p < 0.0001 as calculated by a two-tailed Student’s t test (B, D, and E) or one-way ANOVA multiple comparisons test with Tukey correction (G). Results are combined from at least 2 independent experiments. See also .
Rhil 36r Agonist, supplied by Novoprotein, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/il+36r/36r+agonist+il/pmc12879486-46-12-18
Average 86 stars, based on 1 article reviews
rhil 36r agonist - by Bioz Stars, 2026-10
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N/A
Boster Bio Anti-IL-36R IL1RL2 Antibody (Monoclonal, ABM47A2) (Catalog# M09203). Tested in FACS, WB application(s). This antibody reacts with Human.
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N/A
Interleukin-1 receptor-like 2 is a protein that in humans is encoded by the IL1RL2 gene, belongs to the interleukin-1 receptor family.IL1RL2 is the receptor for interleukin-36 (IL36A, IL36B and IL36G). After binding to interleukin-36 associates
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N/A
Boster Bio Anti-IL-1RL2 / IL-36R Reference Antibody (spesolimab) (Catalog # M09203-1). Tested in Flow Cytometry, ELISA, FTA. This antibody reacts with Cynomolgus monkey, Human. Endotoxin: < 0.960EU/μg,determined by LAL method. Expression system: CHO Cell
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Image Search Results


The treatments targeting of lymphocytes in vivo .

Journal: Frontiers in Physiology

Article Title: Lymphocytes: Versatile Participants in Acute Kidney Injury and Progression to Chronic Kidney Disease

doi: 10.3389/fphys.2021.729084

Figure Lengend Snippet: The treatments targeting of lymphocytes in vivo .

Article Snippet: The administration of an IL-36R antagonist after UUO attenuated tubulointerstitial lesions (TILs) that might be associated with the reduction of Th17 differentiation (Chi et al., ).

Techniques: In Vivo, Activity Assay, Activation Assay, Histone Deacetylase Assay

WT and IL-36R −/− mice dorsal skin was naive or e.c. exposed to S. aureus (1 × 10 8 CFU) for 7 days. Photographs and disease score were taken on day 7, and skin biopsies (10 mm), and lungs were harvested on day 10 ( n ≥ 9 per group). (A) Representative skin photographs. (B) Mean disease score (±SEM). (C) Representative lung and bronchiole histology (H&E, scale bars: 1 mm and 100 μm). (D) Lung inflammation (%) ±SEM from lung sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (E) Mean bronchiole epidermal thickness (±SEM). (F) GO biological process enrichment pathway analysis of RNA-seq from day 10 naive and e.c.-exposed (WT) lungs ( n = 5 per group). resp, responses; reg., regulation; pos., positive; leuk., leukocyte; migr., migration; sig., signaling. (G) Mean number of lung PMNs, monocytes, and eosinophils (±SEM) in day 10 lungs as measured by fluorescence-activated cell sorting (FACS). ns, not significant; ** p < 0.01, *** p < 0.001, and **** p < 0.0001 as calculated by a two-tailed Student’s t test (B, D, and E) or one-way ANOVA multiple comparisons test with Tukey correction (G). Results are combined from at least 2 independent experiments. See also .

Journal: Cell reports

Article Title: Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march

doi: 10.1016/j.celrep.2025.116054

Figure Lengend Snippet: WT and IL-36R −/− mice dorsal skin was naive or e.c. exposed to S. aureus (1 × 10 8 CFU) for 7 days. Photographs and disease score were taken on day 7, and skin biopsies (10 mm), and lungs were harvested on day 10 ( n ≥ 9 per group). (A) Representative skin photographs. (B) Mean disease score (±SEM). (C) Representative lung and bronchiole histology (H&E, scale bars: 1 mm and 100 μm). (D) Lung inflammation (%) ±SEM from lung sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (E) Mean bronchiole epidermal thickness (±SEM). (F) GO biological process enrichment pathway analysis of RNA-seq from day 10 naive and e.c.-exposed (WT) lungs ( n = 5 per group). resp, responses; reg., regulation; pos., positive; leuk., leukocyte; migr., migration; sig., signaling. (G) Mean number of lung PMNs, monocytes, and eosinophils (±SEM) in day 10 lungs as measured by fluorescence-activated cell sorting (FACS). ns, not significant; ** p < 0.01, *** p < 0.001, and **** p < 0.0001 as calculated by a two-tailed Student’s t test (B, D, and E) or one-way ANOVA multiple comparisons test with Tukey correction (G). Results are combined from at least 2 independent experiments. See also .

Article Snippet: Anti-IL-36R mAb , Boehringer Ingelheim ( gary.caviness@boehringer-ingelheim.com ) , .

Techniques: Software, Staining, RNA Sequencing, Migration, Fluorescence, FACS, Two Tailed Test

WT naive (day 0) or WT, K14- IL-36R −/− , and Nkx- IL-36R −/− mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. Photographs and disease score were taken on day 7, skin biopsies (10 mm) were harvested on day 10, and BAL and lungs were harvested on day 13 ( n ≥ 8 per group). (A) Timeline of the atopic march model. (B) Representative skin photographs. (C) Mean disease score (±SEM). (D) Representative skin histology (H&E stain, scale bar: 100 μm). (E) Mean epidermal thickness (±SEM). (F) Representative skin immunofluorescence for IL-36α (green) and DAPI (blue) (scale bar: 100 μm). Dashed line represents the dermo-epidermal junction. (G) Quantification of epidermal IL-36α expression levels from (F) using the raw integrated density measurement in ImageJ, normalized to the epidermal area. (H) Weight change (%) from day 0 to 13 (±SEM). (I) Representative lung histology (H&E; scale bars: 1 mm and 100 μm). (J) Lung inflammation from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining (±SEM). (K) Mean bronchiole epidermal thickness (±SEM). (L) Representative lung immunofluorescence for IL-36α (green) and DAPI (blue) (scale bar: 100 μm). (M) Quantification of lung IL-36α expression levels from (L) using the raw integrated density measurement in ImageJ, normalized to areas of lung cellularity. ns, not significant; ** p < 0.01, *** p < 0.001, and **** p < 0.0001 as calculated by one-way ANOVA multiple comparisons test with Tukey correction (C, E, G, H, J, K, and M). Results are combined from at least 2 independent experiments. See also and .

Journal: Cell reports

Article Title: Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march

doi: 10.1016/j.celrep.2025.116054

Figure Lengend Snippet: WT naive (day 0) or WT, K14- IL-36R −/− , and Nkx- IL-36R −/− mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. Photographs and disease score were taken on day 7, skin biopsies (10 mm) were harvested on day 10, and BAL and lungs were harvested on day 13 ( n ≥ 8 per group). (A) Timeline of the atopic march model. (B) Representative skin photographs. (C) Mean disease score (±SEM). (D) Representative skin histology (H&E stain, scale bar: 100 μm). (E) Mean epidermal thickness (±SEM). (F) Representative skin immunofluorescence for IL-36α (green) and DAPI (blue) (scale bar: 100 μm). Dashed line represents the dermo-epidermal junction. (G) Quantification of epidermal IL-36α expression levels from (F) using the raw integrated density measurement in ImageJ, normalized to the epidermal area. (H) Weight change (%) from day 0 to 13 (±SEM). (I) Representative lung histology (H&E; scale bars: 1 mm and 100 μm). (J) Lung inflammation from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining (±SEM). (K) Mean bronchiole epidermal thickness (±SEM). (L) Representative lung immunofluorescence for IL-36α (green) and DAPI (blue) (scale bar: 100 μm). (M) Quantification of lung IL-36α expression levels from (L) using the raw integrated density measurement in ImageJ, normalized to areas of lung cellularity. ns, not significant; ** p < 0.01, *** p < 0.001, and **** p < 0.0001 as calculated by one-way ANOVA multiple comparisons test with Tukey correction (C, E, G, H, J, K, and M). Results are combined from at least 2 independent experiments. See also and .

Article Snippet: Anti-IL-36R mAb , Boehringer Ingelheim ( gary.caviness@boehringer-ingelheim.com ) , .

Techniques: Staining, Immunofluorescence, Expressing, Software

WT, K14- IL-36R −/− , Nkx- IL-36R −/−, and PMN −/− mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. Blood was collected on day 10, whereas BAL and lungs were harvested on day 13 ( n ≥ 6 per group). (A) GO biological process enrichment pathway analysis of RNA-seq from WT naive and day 13 lungs ( n = 5 per group). (B) Mean number of BAL PMNs (±SEM) as measured by FACS. (C) Representative lung immunofluorescence for Ly6G (green) and DAPI (blue) on day 13 (scale bar: 100 μm). (D) Quantification of lung tissue Ly6G expression levels (±SEM) from (C) using QuPath. (E) Mean number of blood PMNs/mL (±SEM). (F) Weight change (%) from day 0 to 13 (±SEM). (G) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (H) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (I) Mean bronchiole epidermal thickness (±SEM). (J) Mean number of BAL PMNs and monocytes (±SEM) as measured by FACS. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 as calculated by one-way ANOVA multiple comparisons test with Tukey correction (B, D, and E) and a two-tailed Student’s t test (F and H–J). Results are combined from at least 2 independent experiments. See also - .

Journal: Cell reports

Article Title: Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march

doi: 10.1016/j.celrep.2025.116054

Figure Lengend Snippet: WT, K14- IL-36R −/− , Nkx- IL-36R −/−, and PMN −/− mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. Blood was collected on day 10, whereas BAL and lungs were harvested on day 13 ( n ≥ 6 per group). (A) GO biological process enrichment pathway analysis of RNA-seq from WT naive and day 13 lungs ( n = 5 per group). (B) Mean number of BAL PMNs (±SEM) as measured by FACS. (C) Representative lung immunofluorescence for Ly6G (green) and DAPI (blue) on day 13 (scale bar: 100 μm). (D) Quantification of lung tissue Ly6G expression levels (±SEM) from (C) using QuPath. (E) Mean number of blood PMNs/mL (±SEM). (F) Weight change (%) from day 0 to 13 (±SEM). (G) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (H) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (I) Mean bronchiole epidermal thickness (±SEM). (J) Mean number of BAL PMNs and monocytes (±SEM) as measured by FACS. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 as calculated by one-way ANOVA multiple comparisons test with Tukey correction (B, D, and E) and a two-tailed Student’s t test (F and H–J). Results are combined from at least 2 independent experiments. See also - .

Article Snippet: Anti-IL-36R mAb , Boehringer Ingelheim ( gary.caviness@boehringer-ingelheim.com ) , .

Techniques: RNA Sequencing, Immunofluorescence, Expressing, Software, Staining, Two Tailed Test

Mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. BAL and lungs were harvested on day 13 ( n ≥ 8 per group). In some experiments with WT mice, protease inhibitors or vehicle controls were also administered i.t. on days 10, 11, and 12. (A) Venn diagram of unique and overlapping DEGs from RNA-seq of K14- IL-36R −/− and Nkx- IL-36R −/− lungs compared to WT lungs ( n = 5 per group). (B) GO molecular function enrichment pathway analysis of overlapping DEGs from (A). inhib., inhibitor; act., activity. (C) Timeline of the atopic march model using WT mice with administration of protease inhibitors. (D) Weight change (%) from day 0 to 13 (±SEM). (E) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (F) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (G) Mean bronchiole epidermal thickness (±SEM). (H) Mean number of BAL PMNs (±SEM) as measured by FACS. (I–M) WT and NSP −/− mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. BAL and lungs were harvested on day 13 ( n ≥ 8 per group). (I) Weight change (%) from day 0 to 13 (±SEM). (J) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (K) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (L) Mean bronchiole epidermal thickness (±SEM). (M) Mean number of BAL PMNs (±SEM) as measured by FACS. ns, not significant; * p < 0.05, *** p < 0.001, and **** p < 0.0001 as calculated by a two-tailed Student’s t test (D, F–I, and K–M). Results are combined from at least 2 independent experiments. See also .

Journal: Cell reports

Article Title: Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march

doi: 10.1016/j.celrep.2025.116054

Figure Lengend Snippet: Mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. BAL and lungs were harvested on day 13 ( n ≥ 8 per group). In some experiments with WT mice, protease inhibitors or vehicle controls were also administered i.t. on days 10, 11, and 12. (A) Venn diagram of unique and overlapping DEGs from RNA-seq of K14- IL-36R −/− and Nkx- IL-36R −/− lungs compared to WT lungs ( n = 5 per group). (B) GO molecular function enrichment pathway analysis of overlapping DEGs from (A). inhib., inhibitor; act., activity. (C) Timeline of the atopic march model using WT mice with administration of protease inhibitors. (D) Weight change (%) from day 0 to 13 (±SEM). (E) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (F) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (G) Mean bronchiole epidermal thickness (±SEM). (H) Mean number of BAL PMNs (±SEM) as measured by FACS. (I–M) WT and NSP −/− mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. BAL and lungs were harvested on day 13 ( n ≥ 8 per group). (I) Weight change (%) from day 0 to 13 (±SEM). (J) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (K) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (L) Mean bronchiole epidermal thickness (±SEM). (M) Mean number of BAL PMNs (±SEM) as measured by FACS. ns, not significant; * p < 0.05, *** p < 0.001, and **** p < 0.0001 as calculated by a two-tailed Student’s t test (D, F–I, and K–M). Results are combined from at least 2 independent experiments. See also .

Article Snippet: Anti-IL-36R mAb , Boehringer Ingelheim ( gary.caviness@boehringer-ingelheim.com ) , .

Techniques: RNA Sequencing, Inhibition, Activity Assay, Software, Staining, Two Tailed Test

WT, PAD4 −/− , and PMN- IL-36R −/− mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. BAL and lungs were harvested on day 13 ( n ≥ 8 per group). (A) Weight change (%) from day 0 to 13 (±SEM). (B) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (C) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (D) Mean bronchiole epidermal thickness (±SEM). (E) Mean number of BAL PMNs (±SEM) as measured by FACS. (F) Weight change (%) from day 0 to 13 (±SEM). (G) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (H) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (I) Mean bronchiole epidermal thickness (±SEM). (J) Mean number of BAL PMNs (±SEM) as measured by FACS. (K) Representative lung immunofluorescence for Ly6G (red), H3-Cit (green), and DAPI (blue) (scale bar: 100 μm). (L) Quantification of NETs based on the percentage of area of H3-Cit in QuPath using images from (K). ns, not significant; * p < 0.05, ** p < 0.01, and **** p < 0.0001 as calculated by a two-tailed Student’s t test (A, C–F, H–J, and L). Results are combined from at least 2 independent experiments. See also , , and .

Journal: Cell reports

Article Title: Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march

doi: 10.1016/j.celrep.2025.116054

Figure Lengend Snippet: WT, PAD4 −/− , and PMN- IL-36R −/− mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. BAL and lungs were harvested on day 13 ( n ≥ 8 per group). (A) Weight change (%) from day 0 to 13 (±SEM). (B) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (C) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (D) Mean bronchiole epidermal thickness (±SEM). (E) Mean number of BAL PMNs (±SEM) as measured by FACS. (F) Weight change (%) from day 0 to 13 (±SEM). (G) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (H) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (I) Mean bronchiole epidermal thickness (±SEM). (J) Mean number of BAL PMNs (±SEM) as measured by FACS. (K) Representative lung immunofluorescence for Ly6G (red), H3-Cit (green), and DAPI (blue) (scale bar: 100 μm). (L) Quantification of NETs based on the percentage of area of H3-Cit in QuPath using images from (K). ns, not significant; * p < 0.05, ** p < 0.01, and **** p < 0.0001 as calculated by a two-tailed Student’s t test (A, C–F, H–J, and L). Results are combined from at least 2 independent experiments. See also , , and .

Article Snippet: Anti-IL-36R mAb , Boehringer Ingelheim ( gary.caviness@boehringer-ingelheim.com ) , .

Techniques: Software, Staining, Immunofluorescence, Two Tailed Test

WT mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. An anti-IL-36R neutralizing antibody or isotype control were administered on days 7, 9, 10, and 12. BAL and lungs were harvested on day 13 ( n = 8 per group). (A) Timeline of the atopic march model and antibody administration. (B) Representative skin photographs. (C) Mean disease score ±SEM. (D) Weight change (%) from day 0 to 13 (±SEM). (E) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (F) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (G) Mean bronchiole epidermal thickness (±SEM). (H) Mean number of BAL PMNs (±SEM) as measured by FACS. ns, not significant; ** p < 0.01 as calculated by a two-tailed Student’s t test. Results are combined from at least 2 independent experiments.

Journal: Cell reports

Article Title: Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march

doi: 10.1016/j.celrep.2025.116054

Figure Lengend Snippet: WT mice were e.c. exposed to S. aureus + CrA for 7 days, followed by i.t. CrA administration on days 10–12. An anti-IL-36R neutralizing antibody or isotype control were administered on days 7, 9, 10, and 12. BAL and lungs were harvested on day 13 ( n = 8 per group). (A) Timeline of the atopic march model and antibody administration. (B) Representative skin photographs. (C) Mean disease score ±SEM. (D) Weight change (%) from day 0 to 13 (±SEM). (E) Representative lung histology (H&E, scale bars: 1 mm and 100 μm). (F) Lung inflammation (±SEM) from histologic sections as measured by ImageJ software analysis as the percentage of the density of H&E staining. (G) Mean bronchiole epidermal thickness (±SEM). (H) Mean number of BAL PMNs (±SEM) as measured by FACS. ns, not significant; ** p < 0.01 as calculated by a two-tailed Student’s t test. Results are combined from at least 2 independent experiments.

Article Snippet: Anti-IL-36R mAb , Boehringer Ingelheim ( gary.caviness@boehringer-ingelheim.com ) , .

Techniques: Control, Software, Staining, Two Tailed Test