human il 12 (Miltenyi Biotec)
Structured Review
![NK cell proliferation, biogenesis, and metabolic respiration are heightened during active resolution of neovascular lesions (A) scRNA-seq experimental design for 12- to 16-week-old wild-type male mice treated intraperitoneally (i.p.) with PBS or IL-18 and subjected to laser-induced CNV ( n = 4 mice/group, ≥3 lesions/eye). Scale bar: 50 μm. (B) Isolectin B4 analysis of CNV size in RPE/choroid flatmounts ( n = 11 PBS; n = 17 IL-18 [lesions]). (C) UMAP (Scanpy) of CNV tissue from PBS- and IL-18-treated mice ( n = 8 eyes/condition). Bar chart shows treatment-specific cell-type proportions; see also A. (D) Dot plot of known marker genes across cell types. Dot size indicates proportion of cells in cluster expressing a gene; color indicates relative level of expression. (E) UMAP showing predicted cell-cycle phase with summary bar chart of phase distribution per cell type. (F) Top 20 DEGs in NK cells (IL-18 vs. PBS), ranked by Wilcoxon significance; see also B. (G) Dot plot of NK-related genes in NK1 and NK2 populations under PBS or IL-18 treatment. (H) Ncr1 and CD3ε expression in cells from RPE/choroid of mice ( n = 8 eyes). (I) Pou2f2 , Klrg1, Klrk1 , and Klrb1c gene expression in PBS- versus IL-18-treated mice. (J) Functional enrichment analysis of genes differentially upregulated in NK2 vs. NK1 cells in IL-18-treated samples only; see also A. (K and L) Flow cytometry analysis of CNV tissue from 8- to 10-week-old C57Bl/6J mice treated with PBS or IL-18 ( n = 3 mice/group); see B for gating. (M and N) Flow cytometry of CD69 and IFN-γ expression in splenocytes from naive C57Bl/6J mice (8–10 week old) treated ex vivo with PBS or rIL-18 (three mice per group); see C. (O) Seahorse analysis of energetic phenotype of NK cells isolated from C57Bl/6J mouse splenocytes unstimulated vs. <t>IL-2/IL-12</t> pair vs. IL-18 alone. Bar charts presented as mean ± SEM. ∗ p < 0.05, ∗∗ p < 0.01. Following normality testing, unpaired t tests or one-way ANOVA with Dunnett’s multiple comparison tests were used to compare groups.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_3971/pmc13293971/pmc13293971__gr4.jpg)
Human Il 12, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 93/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 42 article reviews
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1) Product Images from "Circulating natural killer cells are phenotypically and functionally altered in age-related macular degeneration"
Article Title: Circulating natural killer cells are phenotypically and functionally altered in age-related macular degeneration
Journal: Cell Reports Medicine
doi: 10.1016/j.xcrm.2026.102792
Figure Legend Snippet: NK cell proliferation, biogenesis, and metabolic respiration are heightened during active resolution of neovascular lesions (A) scRNA-seq experimental design for 12- to 16-week-old wild-type male mice treated intraperitoneally (i.p.) with PBS or IL-18 and subjected to laser-induced CNV ( n = 4 mice/group, ≥3 lesions/eye). Scale bar: 50 μm. (B) Isolectin B4 analysis of CNV size in RPE/choroid flatmounts ( n = 11 PBS; n = 17 IL-18 [lesions]). (C) UMAP (Scanpy) of CNV tissue from PBS- and IL-18-treated mice ( n = 8 eyes/condition). Bar chart shows treatment-specific cell-type proportions; see also A. (D) Dot plot of known marker genes across cell types. Dot size indicates proportion of cells in cluster expressing a gene; color indicates relative level of expression. (E) UMAP showing predicted cell-cycle phase with summary bar chart of phase distribution per cell type. (F) Top 20 DEGs in NK cells (IL-18 vs. PBS), ranked by Wilcoxon significance; see also B. (G) Dot plot of NK-related genes in NK1 and NK2 populations under PBS or IL-18 treatment. (H) Ncr1 and CD3ε expression in cells from RPE/choroid of mice ( n = 8 eyes). (I) Pou2f2 , Klrg1, Klrk1 , and Klrb1c gene expression in PBS- versus IL-18-treated mice. (J) Functional enrichment analysis of genes differentially upregulated in NK2 vs. NK1 cells in IL-18-treated samples only; see also A. (K and L) Flow cytometry analysis of CNV tissue from 8- to 10-week-old C57Bl/6J mice treated with PBS or IL-18 ( n = 3 mice/group); see B for gating. (M and N) Flow cytometry of CD69 and IFN-γ expression in splenocytes from naive C57Bl/6J mice (8–10 week old) treated ex vivo with PBS or rIL-18 (three mice per group); see C. (O) Seahorse analysis of energetic phenotype of NK cells isolated from C57Bl/6J mouse splenocytes unstimulated vs. IL-2/IL-12 pair vs. IL-18 alone. Bar charts presented as mean ± SEM. ∗ p < 0.05, ∗∗ p < 0.01. Following normality testing, unpaired t tests or one-way ANOVA with Dunnett’s multiple comparison tests were used to compare groups.
Techniques Used: Marker, Expressing, Gene Expression, Functional Assay, Flow Cytometry, Ex Vivo, Isolation, Comparison
Figure Legend Snippet: NK cells are found localized adjacent to neovessels in nAMD (A) HRMEC cells were treated for 24 h with 100 μM etoposide and analyzed for expression of markers of cellular senescence ( n = 3). (B) Representative image of β-galactosidase expression in control versus etoposide-treated HRMECs ( n = 3). Scale bar: 200 μm. (C) NKG2DL expression on HRMECs treated with etoposide ( n = 3); see primer list in A. (D–H) NK92MI cells were treated for 18 h with IL-15/18 and incubated with or without HRMECs for 4 h, scale bar: 400 μm, (E) expression of CD107a measured by flow cytometry ( n = 4), (F) cell viability measured by MTS assay ( n = 3), (G) lytic cell death measured by LDH assay ( n = 4), and (H) target cell apoptosis measured by caspase-3/-7 assay ( n = 4). (I) PBMCs were isolated from healthy donors, treated with NK-activating cytokines (IL-12/15 or IL-15/18) for 18 h, and incubated with or without HRMECs for 4 h. Expression of CD107a was measured by flow cytometry ( n = 3–5); see also B. (J and K) Representative and control immunostaining of NCR1 (red) and UEA-1 (green) in cross-sections from non-disease donor controls ( n = 3); see donor information in D. (L) H&E staining in human donor eye with CNV. Orange autofluorescence due to RPE lipofuscin. ∗denotes area of CNV. (M–P) Representative immunostaining of NCR1 (red) and UEA-1 (green) in cross-sections of patients with nAMD ( n = 3); higher magnifications of lesional tissue of one donor shown in Na&b. High-magnification images of two further donors shown in (O) and (M). Closed white arrows denote areas of NCR1 + staining at or adjacent to blood vessels. Open white arrows denote areas of NCR1 + staining in choroidal tissue. Yellow arrows denote areas of NCR1 + staining at the neovascular membrane. Graphical data presented as mean ± SEM. ∗ p < 0.05 ∗∗ p < 0.01, ∗∗∗ p < 0.005, ∗∗∗∗ p < 0.001. Following normality testing, unpaired t tests or one-way ANOVA with Dunnett’s multiple comparison tests were used to compare groups.
Techniques Used: Expressing, Control, Incubation, Flow Cytometry, MTS Assay, Lactate Dehydrogenase Assay, Isolation, Immunostaining, Staining, Membrane, Comparison
Figure Legend Snippet: NK cell immunotherapy reduces neovascular lesion volume and repairs neovessel barrier integrity in models of retinal neovascularization (A) Schematic representation of therapeutic administration of isolated, activated NCR1-GFP − or NCR1-GFP + NK cells in liCNV model in C57Bl/6J mice. (B) RPE/choroid flatmounts from wild-type mice receiving adoptive transfer of IL-12/-15/-18-activated NCR1-GFP − NK cells (top panel) or NCR1-GFP + NK cells were stained for isolectin B4 (red) and DAPI (blue) at 3 days post-liCNV ( n = 4 eyes, 3–4 lesions/eye). Scale bar: 58 μm. (C and D) Schematic representation of therapeutic administration of isolated, activated NK cells in the liCNV model. (D) RPE/choroid flatmounts were stained for isolectin B4 (green) and CNV volume was analyzed by confocal microscopy and IMARIS. n = 5 mice/group, 3 CNVs/eye. Scale bar: 115 μm. (E) Schematic representation of adoptive transfer of isolated, activated C57Bl/6J NK cells in a JR5558 model of spontaneous retinal vascularization ( n = 3–4 mice/group). (E) Fundus fluorescein angiography (FFA) was performed prior to (top), and 5 days following (bottom), NK cell administration. (F) Quantification of leakage area from retinal neovascular lesions. Graphical data presented as mean ± SEM; statistical analysis by unpaired t test or two-way ANOVA with Fisher’s LSD test where ∗ p ≤ 0.05, ∗∗ p < 0.01.
Techniques Used: Isolation, Adoptive Transfer Assay, Staining, Confocal Microscopy
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