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Bio X Cell anti il 1r antibody

Effects of dermal γδT blockade and IL-1 signaling inhibition on skin inflammation in HDM/SEB-treated SSKO mice. A Experimental design for γδTCR antibody (Ab) treatment. IgG was used as a control. B Representative flow cytometry plots for dermal γδT cells (1) and DETCs (2) among CD45 + CD90.2 + cells. The numbers in the plots represent the relative abundance of the indicated cell populations. C Representative images of IgG- or γδTCR Ab-treated SSKO mice on day 11. D Clinical scores of IgG- or γδTCR Ab-treated SSKO mice on day 11. n = 5 mice per group. E Representative skin histology (H&E staining) on day 11. Scale bar = 100 μm. F Quantification of epidermal thickness. n = 5 mice per group. G TEWL values of IgG- or γδTCR Ab-treated SSKO mice on day 11. n = 5 mice per group. H Quantification of the number of the indicated cell types per gram of skin tissue in IgG- or γδTCR Ab-treated SSKO mice on day 11. See the legend of Fig. for additional details. n = 5 mice per group. I , J RT‒qPCR results of the indicated genes in the whole skin of HDM/SEB-treated Ctrl (n = 6) and SSKO (n = 5) mice ( I ) or of IgG- or γδTCR Ab-treated SSKO mice (n = 5 mice per group) on day 11 ( J ). K RT‒qPCR results of Ovol1 and Il1a expression in epidermal cells of HDM/SEB-treated mice on day 7. n = 3 mice per group. L Experimental design for <t>IL-1R</t> Ab treatment (M-S). The samples were harvested on day 11 after treatment for downstream analysis. IgG was used as a control. M Flow cytometry analysis of dermal γδT cells in the back skin of IgG- or IL-1R Ab-treated SSKO mice. See the legend of Fig. for additional details. n = 4 mice per group. N Representative images of IgG- or IL-1R Ab-treated SSKO mice. O Clinical scores of IgG- or IL-1R Ab-treated SSKO mice. n = 5 mice per group. P Representative skin histology (H&E staining). Scale bar = 100 μm. Q Quantification of epidermal thickness in IgG- or IL-1R Ab-treated SSKO mice. n = 4 mice per group. R TEWL values of IgG- or IL-1R Ab-treated SSKO mice. n = 5 mice per group. S RT‒qPCR results showing Il4 , Il17a , and Il33 expression in whole skin. n = 5 mice per group. Data are presented as the means ± SEMs. * p < 0.05, ** p < 0.01, *** p < 0.001. p values were calculated via 2-tailed unpaired Student’s t test or the Mann‒Whitney U tes t

Anti Il 1r Antibody, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 93/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti il 1r antibody/product/Bio X Cell
Average 93 stars, based on 19 article reviews

anti il 1r antibody - by Bioz Stars, 2026-06

93/100 stars

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1) Product Images from "The AhR-Ovol1-Id1 regulatory axis in keratinocytes promotes epidermal and immune homeostasis in atopic dermatitis-like skin inflammation"

Article Title: The AhR-Ovol1-Id1 regulatory axis in keratinocytes promotes epidermal and immune homeostasis in atopic dermatitis-like skin inflammation

Journal: Cellular and Molecular Immunology

doi: 10.1038/s41423-025-01264-z

Figure Legend Snippet: Effects of dermal γδT blockade and IL-1 signaling inhibition on skin inflammation in HDM/SEB-treated SSKO mice. A Experimental design for γδTCR antibody (Ab) treatment. IgG was used as a control. B Representative flow cytometry plots for dermal γδT cells (1) and DETCs (2) among CD45 + CD90.2 + cells. The numbers in the plots represent the relative abundance of the indicated cell populations. C Representative images of IgG- or γδTCR Ab-treated SSKO mice on day 11. D Clinical scores of IgG- or γδTCR Ab-treated SSKO mice on day 11. n = 5 mice per group. E Representative skin histology (H&E staining) on day 11. Scale bar = 100 μm. F Quantification of epidermal thickness. n = 5 mice per group. G TEWL values of IgG- or γδTCR Ab-treated SSKO mice on day 11. n = 5 mice per group. H Quantification of the number of the indicated cell types per gram of skin tissue in IgG- or γδTCR Ab-treated SSKO mice on day 11. See the legend of Fig. for additional details. n = 5 mice per group. I , J RT‒qPCR results of the indicated genes in the whole skin of HDM/SEB-treated Ctrl (n = 6) and SSKO (n = 5) mice ( I ) or of IgG- or γδTCR Ab-treated SSKO mice (n = 5 mice per group) on day 11 ( J ). K RT‒qPCR results of Ovol1 and Il1a expression in epidermal cells of HDM/SEB-treated mice on day 7. n = 3 mice per group. L Experimental design for IL-1R Ab treatment (M-S). The samples were harvested on day 11 after treatment for downstream analysis. IgG was used as a control. M Flow cytometry analysis of dermal γδT cells in the back skin of IgG- or IL-1R Ab-treated SSKO mice. See the legend of Fig. for additional details. n = 4 mice per group. N Representative images of IgG- or IL-1R Ab-treated SSKO mice. O Clinical scores of IgG- or IL-1R Ab-treated SSKO mice. n = 5 mice per group. P Representative skin histology (H&E staining). Scale bar = 100 μm. Q Quantification of epidermal thickness in IgG- or IL-1R Ab-treated SSKO mice. n = 4 mice per group. R TEWL values of IgG- or IL-1R Ab-treated SSKO mice. n = 5 mice per group. S RT‒qPCR results showing Il4 , Il17a , and Il33 expression in whole skin. n = 5 mice per group. Data are presented as the means ± SEMs. * p < 0.05, ** p < 0.01, *** p < 0.001. p values were calculated via 2-tailed unpaired Student’s t test or the Mann‒Whitney U tes t

Techniques Used: Inhibition, Control, Flow Cytometry, Staining, Expressing

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Figure 2. The relative RNA and protein expression of HMGB1, TLR4, IL-1β, IL-1R in epileptogenic tubers (ETs) and non-epileptogenic tubers (non-ETs) (RNA :n = 17; protein: n = 10), and wild-type and control model mice group (n = 6). Figure A showed the relative RNA level of HMGB-1 (1.40 ± 0.32, t(17) = 5.574, P < 0.0001), TLR4 (P = 0.045), IL-1β (P = 0.005), and IL-1R (P = 0.009) were signiﬁcantly lower in non-ETs compared to ETs. Figure B showed the protein level of HMGB-1 (t(18) = 2.617, P = 0.017), TLR4 (t(18) = 3.074, P = 0.007), IL-1β (t(18) = 2.140, P = 0.046), and IL-1R (P = 0.043) were signiﬁcantly lower in non-ETs than ETs. Figure C showed the relative RNA level of HMGB-1 (P = 0.004), TLR4 (t(10) = 4.179, P = 0.002), IL-1β (t(10) = 6.411, P < 0.0001), and IL-1R (P = 0.004) were signiﬁcantly lower in wild-type control group compared to model control group. Figure D showed the protein level of HMGB-1 (t(10) = 4.461, P = 0.001), TLR4 (t(10) = 6.558, P < 0.0001), IL-1β (t(10) = 3.449, P = 0.006), and IL-1R (t(10) = 6.108, P = 0.0001) were signiﬁcantly lower in wild-type control group compared to model control group (*: p < 0.05; **: p < 0.01; ***: p < 0.001; ****p < 0.0001).

Journal: Science progress

Article Title: HMGB1 mediates inflammation response of epileptogenicity in tuberous sclerosis complex-related epilepsy.

doi: 10.1177/00368504251338653

Figure Lengend Snippet: Figure 2. The relative RNA and protein expression of HMGB1, TLR4, IL-1β, IL-1R in epileptogenic tubers (ETs) and non-epileptogenic tubers (non-ETs) (RNA :n = 17; protein: n = 10), and wild-type and control model mice group (n = 6). Figure A showed the relative RNA level of HMGB-1 (1.40 ± 0.32, t(17) = 5.574, P < 0.0001), TLR4 (P = 0.045), IL-1β (P = 0.005), and IL-1R (P = 0.009) were signiﬁcantly lower in non-ETs compared to ETs. Figure B showed the protein level of HMGB-1 (t(18) = 2.617, P = 0.017), TLR4 (t(18) = 3.074, P = 0.007), IL-1β (t(18) = 2.140, P = 0.046), and IL-1R (P = 0.043) were signiﬁcantly lower in non-ETs than ETs. Figure C showed the relative RNA level of HMGB-1 (P = 0.004), TLR4 (t(10) = 4.179, P = 0.002), IL-1β (t(10) = 6.411, P < 0.0001), and IL-1R (P = 0.004) were signiﬁcantly lower in wild-type control group compared to model control group. Figure D showed the protein level of HMGB-1 (t(10) = 4.461, P = 0.001), TLR4 (t(10) = 6.558, P < 0.0001), IL-1β (t(10) = 3.449, P = 0.006), and IL-1R (t(10) = 6.108, P = 0.0001) were signiﬁcantly lower in wild-type control group compared to model control group (*: p < 0.05; **: p < 0.01; ***: p < 0.001; ****p < 0.0001).

Article Snippet: The primary antibodies HMGB1 (1:250; Abcam; cat. no. ab79823), TLR4 (1:100; Abcam; cat. no. ab22048), IL-1β (1:50; Abcam; cat. no. ab315084), and IL-1R (1:50; Santa Cruz Biotechnology; cat. no. sc-66054) were incubated overnight at 4°C.

Techniques: Expressing, Control

Figure 3. Immunoﬂuorescence of HMGB1,TLR4, lL-1β and IL-1R in ETs and non-ETs. Positive expression of HMGB1 is green, and positive expression of TLR4 is red on the image of immunoﬂuorescence in ETs and non-ETs (Figure 3A, magniﬁcations: × 4 and ×40). The percentages of positive cells (positive area) (n = 9) of HMGB1 (t(16) = 2.770, P = 0.014) and TLR4 (t(16) = 4.884, P = 0.0002)were larger in ETs than them in non-ETs (Figure 3B) and, the ﬂuorescence intensity (n = 15) of either HMGB1 (t(28) = 2.285, P = 0.030) or TLR4 (t(28) = 2.857, P = 0.008) was higher in ETs than them in non-ETs (Figure 3C). Positive expression of IL-1β is green, and positive expression of IL-1R is red on the image of immunoﬂuorescence in ETs and non-ETs (Figure 3D, magniﬁcations: × 4 and ×40). The positive area (n = 9) of IL-1R (P = 0.031) was larger in ETs than non-ETs (Figure 3E), and the ﬂuorescence intensity (n = 15) of either IL-1β (t(28) = 5.055, P < 0.0001) or IL-1R (t(28) = 2.111, P = 0.043) were higher in ETs non-ETs (Figure 3F).

Journal: Science progress

Article Title: HMGB1 mediates inflammation response of epileptogenicity in tuberous sclerosis complex-related epilepsy.

doi: 10.1177/00368504251338653

Figure Lengend Snippet: Figure 3. Immunoﬂuorescence of HMGB1,TLR4, lL-1β and IL-1R in ETs and non-ETs. Positive expression of HMGB1 is green, and positive expression of TLR4 is red on the image of immunoﬂuorescence in ETs and non-ETs (Figure 3A, magniﬁcations: × 4 and ×40). The percentages of positive cells (positive area) (n = 9) of HMGB1 (t(16) = 2.770, P = 0.014) and TLR4 (t(16) = 4.884, P = 0.0002)were larger in ETs than them in non-ETs (Figure 3B) and, the ﬂuorescence intensity (n = 15) of either HMGB1 (t(28) = 2.285, P = 0.030) or TLR4 (t(28) = 2.857, P = 0.008) was higher in ETs than them in non-ETs (Figure 3C). Positive expression of IL-1β is green, and positive expression of IL-1R is red on the image of immunoﬂuorescence in ETs and non-ETs (Figure 3D, magniﬁcations: × 4 and ×40). The positive area (n = 9) of IL-1R (P = 0.031) was larger in ETs than non-ETs (Figure 3E), and the ﬂuorescence intensity (n = 15) of either IL-1β (t(28) = 5.055, P < 0.0001) or IL-1R (t(28) = 2.111, P = 0.043) were higher in ETs non-ETs (Figure 3F).

Techniques: Expressing

Figure 4. The expression pattern of relative RNA and protein of HMGB1, TLR4, IL-1β, IL-1R, and the frequency of abnormal discharge and seizure attacks in mouse model. (red line: P50; blue line: P57). Figure (5A-5D) shows the relative RNA content of HMGB-1, TLR4, IL-1β and IL-1R in wild-type control group, model control group, HMGB1 prevention group, IL-1β prevention group, HMGB1 intervention group, and IL-1β intervention group. The relative RNA content of IL-1β in HMGB1-intervention group was lower compared to model control group (t(10)=2.645, P =0.025) and higher than wild-type group. Figure (5E-5H) showed the protein levels of HMGB-1, TLR4, IL-1β and IL-1R in wild-type control group, model control group, HMGB1 prevention group, IL-1β prevention group, HMGB1 intervention group, and IL-1β intervention group. The protein content of HMGB1 (t(10) =4.461, P=0.001), TLR4 (t(10) = 6.558, P<0.0001), IL-1β (t(10)=3.449, P<0.006), and IL-1R (t(10) =6.108, P=0.001) in wild-type control group was signiﬁcantly lower than model control group. Figure (5I-5J): The frequency of seizure attacks at P50 in the HMGB1- prevention (P =0.007) and -intervention (P=0.027) groups was signiﬁcantly decreased compared with the model control group. The frequency of seizure attacks at P50 in the IL-1β- prevention (P=0.009) and -intervention (P=0.046) groups were signiﬁcantly decreased compared with the model control group. The frequency of abnormal discharge on EEG at P50 in the HMGB1- prevention (P=0.007) and -intervention (P =0.023) groups were signiﬁcantly decreased compared with the model control group. The frequency of abnormal discharge on EEG at P50 in the IL-1β- prevention (P=0.002) and -intervention (P=0.011) groups were signiﬁcantly decreased compared with the model control group. The frequency of abnormal discharge on EEG (P< 0.0001) and seizure attacks (P=0.0004) at P50 in the wild-type control group were signiﬁcantly decreased compared with the model control group. The frequency of abnormal discharge on EEG (P =0.018) and seizure attacks (P=0.021) at P57 in the wild-type control group were signiﬁcantly decreased compared with the model control group (*: p<0.05; **: p<0.01; ***: p<0.001; ****p< 0.0001).

Journal: Science progress

Article Title: HMGB1 mediates inflammation response of epileptogenicity in tuberous sclerosis complex-related epilepsy.

doi: 10.1177/00368504251338653

Figure Lengend Snippet: Figure 4. The expression pattern of relative RNA and protein of HMGB1, TLR4, IL-1β, IL-1R, and the frequency of abnormal discharge and seizure attacks in mouse model. (red line: P50; blue line: P57). Figure (5A-5D) shows the relative RNA content of HMGB-1, TLR4, IL-1β and IL-1R in wild-type control group, model control group, HMGB1 prevention group, IL-1β prevention group, HMGB1 intervention group, and IL-1β intervention group. The relative RNA content of IL-1β in HMGB1-intervention group was lower compared to model control group (t(10)=2.645, P =0.025) and higher than wild-type group. Figure (5E-5H) showed the protein levels of HMGB-1, TLR4, IL-1β and IL-1R in wild-type control group, model control group, HMGB1 prevention group, IL-1β prevention group, HMGB1 intervention group, and IL-1β intervention group. The protein content of HMGB1 (t(10) =4.461, P=0.001), TLR4 (t(10) = 6.558, P<0.0001), IL-1β (t(10)=3.449, P<0.006), and IL-1R (t(10) =6.108, P=0.001) in wild-type control group was signiﬁcantly lower than model control group. Figure (5I-5J): The frequency of seizure attacks at P50 in the HMGB1- prevention (P =0.007) and -intervention (P=0.027) groups was signiﬁcantly decreased compared with the model control group. The frequency of seizure attacks at P50 in the IL-1β- prevention (P=0.009) and -intervention (P=0.046) groups were signiﬁcantly decreased compared with the model control group. The frequency of abnormal discharge on EEG at P50 in the HMGB1- prevention (P=0.007) and -intervention (P =0.023) groups were signiﬁcantly decreased compared with the model control group. The frequency of abnormal discharge on EEG at P50 in the IL-1β- prevention (P=0.002) and -intervention (P=0.011) groups were signiﬁcantly decreased compared with the model control group. The frequency of abnormal discharge on EEG (P< 0.0001) and seizure attacks (P=0.0004) at P50 in the wild-type control group were signiﬁcantly decreased compared with the model control group. The frequency of abnormal discharge on EEG (P =0.018) and seizure attacks (P=0.021) at P57 in the wild-type control group were signiﬁcantly decreased compared with the model control group (*: p<0.05; **: p<0.01; ***: p<0.001; ****p< 0.0001).

Techniques: Expressing, Control

Journal: Cellular and Molecular Immunology

Article Title: The AhR-Ovol1-Id1 regulatory axis in keratinocytes promotes epidermal and immune homeostasis in atopic dermatitis-like skin inflammation

doi: 10.1038/s41423-025-01264-z

Figure Lengend Snippet: Effects of dermal γδT blockade and IL-1 signaling inhibition on skin inflammation in HDM/SEB-treated SSKO mice. A Experimental design for γδTCR antibody (Ab) treatment. IgG was used as a control. B Representative flow cytometry plots for dermal γδT cells (1) and DETCs (2) among CD45 + CD90.2 + cells. The numbers in the plots represent the relative abundance of the indicated cell populations. C Representative images of IgG- or γδTCR Ab-treated SSKO mice on day 11. D Clinical scores of IgG- or γδTCR Ab-treated SSKO mice on day 11. n = 5 mice per group. E Representative skin histology (H&E staining) on day 11. Scale bar = 100 μm. F Quantification of epidermal thickness. n = 5 mice per group. G TEWL values of IgG- or γδTCR Ab-treated SSKO mice on day 11. n = 5 mice per group. H Quantification of the number of the indicated cell types per gram of skin tissue in IgG- or γδTCR Ab-treated SSKO mice on day 11. See the legend of Fig. for additional details. n = 5 mice per group. I , J RT‒qPCR results of the indicated genes in the whole skin of HDM/SEB-treated Ctrl (n = 6) and SSKO (n = 5) mice ( I ) or of IgG- or γδTCR Ab-treated SSKO mice (n = 5 mice per group) on day 11 ( J ). K RT‒qPCR results of Ovol1 and Il1a expression in epidermal cells of HDM/SEB-treated mice on day 7. n = 3 mice per group. L Experimental design for IL-1R Ab treatment (M-S). The samples were harvested on day 11 after treatment for downstream analysis. IgG was used as a control. M Flow cytometry analysis of dermal γδT cells in the back skin of IgG- or IL-1R Ab-treated SSKO mice. See the legend of Fig. for additional details. n = 4 mice per group. N Representative images of IgG- or IL-1R Ab-treated SSKO mice. O Clinical scores of IgG- or IL-1R Ab-treated SSKO mice. n = 5 mice per group. P Representative skin histology (H&E staining). Scale bar = 100 μm. Q Quantification of epidermal thickness in IgG- or IL-1R Ab-treated SSKO mice. n = 4 mice per group. R TEWL values of IgG- or IL-1R Ab-treated SSKO mice. n = 5 mice per group. S RT‒qPCR results showing Il4 , Il17a , and Il33 expression in whole skin. n = 5 mice per group. Data are presented as the means ± SEMs. * p < 0.05, ** p < 0.01, *** p < 0.001. p values were calculated via 2-tailed unpaired Student’s t test or the Mann‒Whitney U tes t

Article Snippet: For IL-1R blocking, the mice were i.p. injected with 200 μg of an anti-IL-1R antibody (BioXcell, Cat# BE0256; Clone JAMA-147) or IgG (BioXcell, Cat# BE0091) at days -1, 0, 3, 7 and 10 of HDM/SEB treatment.

Techniques: Inhibition, Control, Flow Cytometry, Staining, Expressing

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1) Product Images from "The AhR-Ovol1-Id1 regulatory axis in keratinocytes promotes epidermal and immune homeostasis in atopic dermatitis-like skin inflammation"

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