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R&D Systems omcpmutil 2

CD25 (IL-2Rα) and NKG2D were immobilized to individual flow cells of a sensor chip by primary amine chemistry. Serial dilutions of IL-2, mutIL-2, and <t>OMCPmutIL-2</t> were injected across each flow cell and association and dissociation phases were measured. Renditioned graphic model of protein binding (left) with experimental binding to CD25 (middle) and NKG2D (right) for wild type human IL-2 (A), mutant human (R38A, F42K) IL-2 (B), and OMCPmutIL-2 (C). Experimental binding curves are shown for a representative experiment. (D) For binding of CD25:wild-type IL-2 and OMCPmutIL-2:NKG2D experimental curves were fitted using ANABEL software and the observed binding constant (Kobs) was measured for each concentration. The plot of Kobs vs concentration is shown with the slope as the association rate (Kon) and y-axis intercept as the dissociation rate (Koff).

Omcpmutil 2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 91/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 91 stars, based on 8 article reviews

omcpmutil 2 - by Bioz Stars, 2026-03

91/100 stars

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1) Product Images from "Retargeting Interleukin-2 Signaling to NKG2D-Expressing Tumor Infiltrating Leukocytes Improves Adoptive Transfer Immunotherapy"

Article Title: Retargeting Interleukin-2 Signaling to NKG2D-Expressing Tumor Infiltrating Leukocytes Improves Adoptive Transfer Immunotherapy

Journal: Journal of immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.2000926

CD25 (IL-2Rα) and NKG2D were immobilized to individual flow cells of a sensor chip by primary amine chemistry. Serial dilutions of IL-2, mutIL-2, and OMCPmutIL-2 were injected across each flow cell and association and dissociation phases were measured. Renditioned graphic model of protein binding (left) with experimental binding to CD25 (middle) and NKG2D (right) for wild type human IL-2 (A), mutant human (R38A, F42K) IL-2 (B), and OMCPmutIL-2 (C). Experimental binding curves are shown for a representative experiment. (D) For binding of CD25:wild-type IL-2 and OMCPmutIL-2:NKG2D experimental curves were fitted using ANABEL software and the observed binding constant (Kobs) was measured for each concentration. The plot of Kobs vs concentration is shown with the slope as the association rate (Kon) and y-axis intercept as the dissociation rate (Koff).

Figure Legend Snippet: CD25 (IL-2Rα) and NKG2D were immobilized to individual flow cells of a sensor chip by primary amine chemistry. Serial dilutions of IL-2, mutIL-2, and OMCPmutIL-2 were injected across each flow cell and association and dissociation phases were measured. Renditioned graphic model of protein binding (left) with experimental binding to CD25 (middle) and NKG2D (right) for wild type human IL-2 (A), mutant human (R38A, F42K) IL-2 (B), and OMCPmutIL-2 (C). Experimental binding curves are shown for a representative experiment. (D) For binding of CD25:wild-type IL-2 and OMCPmutIL-2:NKG2D experimental curves were fitted using ANABEL software and the observed binding constant (Kobs) was measured for each concentration. The plot of Kobs vs concentration is shown with the slope as the association rate (Kon) and y-axis intercept as the dissociation rate (Koff).

Techniques Used: Injection, Protein Binding, Binding Assay, Mutagenesis, Software, Concentration Assay

(A) Fold TIL expansion of murine B16ova -resident leucocytes. (B) Surface expression of NKG2D and IL-2R alpha chain on mouse antigen specific CD8+ T cells compared to those with ovalbumin non-reactive TCR. (C) Fold TIL expansion of Human melanoma -derived TILS in either wild-type IL-2 (blue) or OMCPmutIL-2 (red) (C). *p<.05; **p<.01, ***p<.001, NS p>.05

Figure Legend Snippet: (A) Fold TIL expansion of murine B16ova -resident leucocytes. (B) Surface expression of NKG2D and IL-2R alpha chain on mouse antigen specific CD8+ T cells compared to those with ovalbumin non-reactive TCR. (C) Fold TIL expansion of Human melanoma -derived TILS in either wild-type IL-2 (blue) or OMCPmutIL-2 (red) (C). *p<.05; **p<.01, ***p<.001, NS p>.05

Techniques Used: Expressing, Derivative Assay

(A) Number of TIL leucocytes transferred into CD45.1 congenic tumor-bearing recipients after expansion in either wild-type IL-2 or OMCPmutIL-2. Flow cytometric analysis performed 24 hours after transfer. (B)Immunohistochemical analysis of B16ova tumors in wild-type C57Bl/6 mice injected with 20×106 TILs from C57Bl/6EGFP mice expanded for 2 weeks in either wild-type IL-2 or OMCPmutIL-2. Histologic evaluation performed 120 hours after transfer. (C) Relative expression, by median fluorescence intensity, of LFA-1, CD49a or CXCR3 on TIL-resident CD8+ T cells, NK cells or gamma delta T cells after 2-week expansion in IL-2 (blue) or OMCPmutIL-2 (red). (D) Relative expression, by median fluorescence intensity, of LFA-1 on TIL-resident CD8+ T cells, NK cells or γδ T cells after either MDSC or Treg depletion prior to expansion in IL-2 (blue) or OMCPmutIL-2 (red). *p<.05; **p<.01, ***p<.001, NS p>.05

Figure Legend Snippet: (A) Number of TIL leucocytes transferred into CD45.1 congenic tumor-bearing recipients after expansion in either wild-type IL-2 or OMCPmutIL-2. Flow cytometric analysis performed 24 hours after transfer. (B)Immunohistochemical analysis of B16ova tumors in wild-type C57Bl/6 mice injected with 20×106 TILs from C57Bl/6EGFP mice expanded for 2 weeks in either wild-type IL-2 or OMCPmutIL-2. Histologic evaluation performed 120 hours after transfer. (C) Relative expression, by median fluorescence intensity, of LFA-1, CD49a or CXCR3 on TIL-resident CD8+ T cells, NK cells or gamma delta T cells after 2-week expansion in IL-2 (blue) or OMCPmutIL-2 (red). (D) Relative expression, by median fluorescence intensity, of LFA-1 on TIL-resident CD8+ T cells, NK cells or γδ T cells after either MDSC or Treg depletion prior to expansion in IL-2 (blue) or OMCPmutIL-2 (red). *p<.05; **p<.01, ***p<.001, NS p>.05

Techniques Used: Immunohistochemical staining, Injection, Expressing, Fluorescence

(A) NKG2D expression in CD8+ TILs. (B) Expansion of NKG2Dlow or NKG2Dhigh CD8+ T cells in OMCPmutIL-2 or wild-type IL-2. (C) Expression of NKG2D (top), perforin (middle), and FasLigand (bottom) on flow cytometrically sorted NKG2Dlow CD8+ T cells immediately post sort (black line bar open circles), after 7 days of culture in wild-type IL-2 (blue bar, open circles) or OMCPmutIL-2 (red bar, open circles). ***p<.001

Figure Legend Snippet: (A) NKG2D expression in CD8+ TILs. (B) Expansion of NKG2Dlow or NKG2Dhigh CD8+ T cells in OMCPmutIL-2 or wild-type IL-2. (C) Expression of NKG2D (top), perforin (middle), and FasLigand (bottom) on flow cytometrically sorted NKG2Dlow CD8+ T cells immediately post sort (black line bar open circles), after 7 days of culture in wild-type IL-2 (blue bar, open circles) or OMCPmutIL-2 (red bar, open circles). ***p<.001

Techniques Used: Expressing

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Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Retargeting Interleukin-2 Signaling to NKG2D-Expressing Tumor Infiltrating Leukocytes Improves Adoptive Transfer Immunotherapy

doi: 10.4049/jimmunol.2000926

Figure Lengend Snippet: CD25 (IL-2Rα) and NKG2D were immobilized to individual flow cells of a sensor chip by primary amine chemistry. Serial dilutions of IL-2, mutIL-2, and OMCPmutIL-2 were injected across each flow cell and association and dissociation phases were measured. Renditioned graphic model of protein binding (left) with experimental binding to CD25 (middle) and NKG2D (right) for wild type human IL-2 (A), mutant human (R38A, F42K) IL-2 (B), and OMCPmutIL-2 (C). Experimental binding curves are shown for a representative experiment. (D) For binding of CD25:wild-type IL-2 and OMCPmutIL-2:NKG2D experimental curves were fitted using ANABEL software and the observed binding constant (Kobs) was measured for each concentration. The plot of Kobs vs concentration is shown with the slope as the association rate (Kon) and y-axis intercept as the dissociation rate (Koff).

Article Snippet: Surface plasmon resonance (SPR) A ProteOn XPR36 instrument (BioRad) was used to determine the kinetics of interaction of WT IL-2, mutIL-2, and OMCPmutIL-2 for murine CD25 (#2438-RM, R&D systems) and murine NKG2D-Fc (#139-NK-050, R&D systems).

Techniques: Injection, Protein Binding, Binding Assay, Mutagenesis, Software, Concentration Assay

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Retargeting Interleukin-2 Signaling to NKG2D-Expressing Tumor Infiltrating Leukocytes Improves Adoptive Transfer Immunotherapy

doi: 10.4049/jimmunol.2000926

Figure Lengend Snippet: (A) Fold TIL expansion of murine B16ova -resident leucocytes. (B) Surface expression of NKG2D and IL-2R alpha chain on mouse antigen specific CD8+ T cells compared to those with ovalbumin non-reactive TCR. (C) Fold TIL expansion of Human melanoma -derived TILS in either wild-type IL-2 (blue) or OMCPmutIL-2 (red) (C). *p<.05; **p<.01, ***p<.001, NS p>.05

Techniques: Expressing, Derivative Assay

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Retargeting Interleukin-2 Signaling to NKG2D-Expressing Tumor Infiltrating Leukocytes Improves Adoptive Transfer Immunotherapy

doi: 10.4049/jimmunol.2000926

Figure Lengend Snippet: (A) Number of TIL leucocytes transferred into CD45.1 congenic tumor-bearing recipients after expansion in either wild-type IL-2 or OMCPmutIL-2. Flow cytometric analysis performed 24 hours after transfer. (B)Immunohistochemical analysis of B16ova tumors in wild-type C57Bl/6 mice injected with 20×106 TILs from C57Bl/6EGFP mice expanded for 2 weeks in either wild-type IL-2 or OMCPmutIL-2. Histologic evaluation performed 120 hours after transfer. (C) Relative expression, by median fluorescence intensity, of LFA-1, CD49a or CXCR3 on TIL-resident CD8+ T cells, NK cells or gamma delta T cells after 2-week expansion in IL-2 (blue) or OMCPmutIL-2 (red). (D) Relative expression, by median fluorescence intensity, of LFA-1 on TIL-resident CD8+ T cells, NK cells or γδ T cells after either MDSC or Treg depletion prior to expansion in IL-2 (blue) or OMCPmutIL-2 (red). *p<.05; **p<.01, ***p<.001, NS p>.05

Techniques: Immunohistochemical staining, Injection, Expressing, Fluorescence

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Retargeting Interleukin-2 Signaling to NKG2D-Expressing Tumor Infiltrating Leukocytes Improves Adoptive Transfer Immunotherapy

doi: 10.4049/jimmunol.2000926

Figure Lengend Snippet: (A) NKG2D expression in CD8+ TILs. (B) Expansion of NKG2Dlow or NKG2Dhigh CD8+ T cells in OMCPmutIL-2 or wild-type IL-2. (C) Expression of NKG2D (top), perforin (middle), and FasLigand (bottom) on flow cytometrically sorted NKG2Dlow CD8+ T cells immediately post sort (black line bar open circles), after 7 days of culture in wild-type IL-2 (blue bar, open circles) or OMCPmutIL-2 (red bar, open circles). ***p<.001

Techniques: Expressing

( A ) Schematic rendition of OMCPmutIL-2 binding to cell surface and variability in common γ chain cytokine surface receptor capture, relying on high-affinity α chain in cis for IL-2 and in trans for IL-15. ( B ) Experimental design and expansion of peripheral blood lymphocyte–derived (PBL-derived) naive CD8 + CD44 lo 62L hi murine T cells as measured by fold expansion and viability. Apoptotic cells defined as Annexin viability dye – and nonviable cells defined as Annexin viability dye + . ( C ) Expression of exhaustion markers on cells expanded in respective cytokines. * P < 0.05; ** P < 0.01; *** P < 0.001; t test. CTLA-4, cytotoxic T lymphocyte–associated protein 4; Lag-3, lymphocyte activating 3; PD-1, programmed cell death 1.

Journal: JCI Insight

Article Title: A reengineered common chain cytokine augments CD8 + T cell–dependent immunotherapy

doi: 10.1172/jci.insight.158889

Figure Lengend Snippet: ( A ) Schematic rendition of OMCPmutIL-2 binding to cell surface and variability in common γ chain cytokine surface receptor capture, relying on high-affinity α chain in cis for IL-2 and in trans for IL-15. ( B ) Experimental design and expansion of peripheral blood lymphocyte–derived (PBL-derived) naive CD8 + CD44 lo 62L hi murine T cells as measured by fold expansion and viability. Apoptotic cells defined as Annexin viability dye – and nonviable cells defined as Annexin viability dye + . ( C ) Expression of exhaustion markers on cells expanded in respective cytokines. * P < 0.05; ** P < 0.01; *** P < 0.001; t test. CTLA-4, cytotoxic T lymphocyte–associated protein 4; Lag-3, lymphocyte activating 3; PD-1, programmed cell death 1.

Article Snippet: Both wild-type human IL-2 and OMCPmutIL-2 were produced through transient transfection in CHO cell line (Celltheon) based on previously described methods ( ).

Techniques: Binding Assay, Derivative Assay, Expressing

( A ) Heatmap showing relative gene expression of memory-driving transcription factors. ( B ) Relative proportion and number of CD44 lo 62L hi naive, CD44 hi 62L hi central memory (Tcm), or CD44 hi 62L lo effector cells (Teff) after 2 weeks of expansion in IL-2 (blue), IL-15 (green), or OMCPmutIL-2 (red). Representative FACS plots (top), quantitative percentage (bottom left), and total cell count (bottom right) from a starting population of 1 × 10 6 flow cytometrically sorted naive cells. ( C ) Analysis of spleen 50 days after adoptive transfer of CD45.2 congenic CD8 + T cells expanded in wild-type IL-2 (blue), IL-15 (green), or OMCPmutIL-2 (red) prior to transfer. ( D ) In vitro cytotoxicity by murine pmel anti-GP100 TCR-transgenic CD8 + T cells as determined by the ability to lyse B16 melanoma (nonviable) and T cell degranulation measured by surface CD107a expression with 1:1 B16/pmel CD8 + T cell ratio. ( E ) Effector cytokine (IFN-γ and TNF-α) production by murine pmel anti-GP100 TCR-transgenic CD8 + T cells expanded in respective cytokines, upon maximal stimulation. ** P < 0.01; *** P < 0.001; t test.

Journal: JCI Insight

Article Title: A reengineered common chain cytokine augments CD8 + T cell–dependent immunotherapy

doi: 10.1172/jci.insight.158889

Figure Lengend Snippet: ( A ) Heatmap showing relative gene expression of memory-driving transcription factors. ( B ) Relative proportion and number of CD44 lo 62L hi naive, CD44 hi 62L hi central memory (Tcm), or CD44 hi 62L lo effector cells (Teff) after 2 weeks of expansion in IL-2 (blue), IL-15 (green), or OMCPmutIL-2 (red). Representative FACS plots (top), quantitative percentage (bottom left), and total cell count (bottom right) from a starting population of 1 × 10 6 flow cytometrically sorted naive cells. ( C ) Analysis of spleen 50 days after adoptive transfer of CD45.2 congenic CD8 + T cells expanded in wild-type IL-2 (blue), IL-15 (green), or OMCPmutIL-2 (red) prior to transfer. ( D ) In vitro cytotoxicity by murine pmel anti-GP100 TCR-transgenic CD8 + T cells as determined by the ability to lyse B16 melanoma (nonviable) and T cell degranulation measured by surface CD107a expression with 1:1 B16/pmel CD8 + T cell ratio. ( E ) Effector cytokine (IFN-γ and TNF-α) production by murine pmel anti-GP100 TCR-transgenic CD8 + T cells expanded in respective cytokines, upon maximal stimulation. ** P < 0.01; *** P < 0.001; t test.

Article Snippet: Both wild-type human IL-2 and OMCPmutIL-2 were produced through transient transfection in CHO cell line (Celltheon) based on previously described methods ( ).

Techniques: Expressing, Cell Counting, Adoptive Transfer Assay, In Vitro, Transgenic Assay

( A ) Canonical signaling pathways described for common γ chain cytokines. ( B ) JAK1 and JAK3 total and phosphorylated levels by Western blot analysis after in vitro activation with anti-CD3/28 stimulation and in the presence of IL-2, IL-15, OMCPmutIL-2, or control (saline). ( C ) Phospho-STAT5 levels in CD8 + T cells activated with IL-2, IL-15, OMCPmutIL-2, or saline control in the presence of anti-CD3/28. * P < 0.05; ** P < 0.01; *** P < 0.001; t test.

Journal: JCI Insight

Article Title: A reengineered common chain cytokine augments CD8 + T cell–dependent immunotherapy

doi: 10.1172/jci.insight.158889

Figure Lengend Snippet: ( A ) Canonical signaling pathways described for common γ chain cytokines. ( B ) JAK1 and JAK3 total and phosphorylated levels by Western blot analysis after in vitro activation with anti-CD3/28 stimulation and in the presence of IL-2, IL-15, OMCPmutIL-2, or control (saline). ( C ) Phospho-STAT5 levels in CD8 + T cells activated with IL-2, IL-15, OMCPmutIL-2, or saline control in the presence of anti-CD3/28. * P < 0.05; ** P < 0.01; *** P < 0.001; t test.

Article Snippet: Both wild-type human IL-2 and OMCPmutIL-2 were produced through transient transfection in CHO cell line (Celltheon) based on previously described methods ( ).

Techniques: Western Blot, In Vitro, Activation Assay

( A ) STAT5 localization by confocal microscopy after in vitro activation with anti-CD3/28 stimulation in the presence of IL-2, IL-15, OMCPmutIL-2, or saline control. Original magnification, 20× (top) and 63× (bottom). ( B ) Gene enrichment analysis for STAT5-dependent genes in memory T cells generated from naive cells in vitro in the presence of IL-2 or IL-15 versus OMCPmutIL-2. ( C ) Principal component analysis between IL-2 (blue), IL-15 (green), and OMCPmutIL-2 (red) and differential gene expression in murine splenic CD8 + T cells expanded in IL-2, IL-15, or OMCPmutIL-2 as expressed via Venn diagram and Kyoto Encyclopedia of Genes and Genomes pathway analysis comparing top differential pathways. OMCPmutIL-2 versus IL-2 and OMCPmutIL-2 versus IL-15 are presented in separate graphs (purple for OMCPmutIL-2 vs. IL-2 and orange for OMCPmutIL-2 vs. IL-15). ( D ) Phosphorylated (inactive) NFAT quantification in CD8 + T cells after expansion in various cytokines. ( E ) Change in CD8 + T cell expansion and cytotoxicity in the presence or absence of NFAT inhibitor FK506. ( F ) Change in CD8 + T cell proliferation and cytokine production in the presence or absence of NFAT inhibitor FK506. * P < 0.05; ** P < 0.01; *** P < 0.001; t test.

Journal: JCI Insight

Article Title: A reengineered common chain cytokine augments CD8 + T cell–dependent immunotherapy

doi: 10.1172/jci.insight.158889

Figure Lengend Snippet: ( A ) STAT5 localization by confocal microscopy after in vitro activation with anti-CD3/28 stimulation in the presence of IL-2, IL-15, OMCPmutIL-2, or saline control. Original magnification, 20× (top) and 63× (bottom). ( B ) Gene enrichment analysis for STAT5-dependent genes in memory T cells generated from naive cells in vitro in the presence of IL-2 or IL-15 versus OMCPmutIL-2. ( C ) Principal component analysis between IL-2 (blue), IL-15 (green), and OMCPmutIL-2 (red) and differential gene expression in murine splenic CD8 + T cells expanded in IL-2, IL-15, or OMCPmutIL-2 as expressed via Venn diagram and Kyoto Encyclopedia of Genes and Genomes pathway analysis comparing top differential pathways. OMCPmutIL-2 versus IL-2 and OMCPmutIL-2 versus IL-15 are presented in separate graphs (purple for OMCPmutIL-2 vs. IL-2 and orange for OMCPmutIL-2 vs. IL-15). ( D ) Phosphorylated (inactive) NFAT quantification in CD8 + T cells after expansion in various cytokines. ( E ) Change in CD8 + T cell expansion and cytotoxicity in the presence or absence of NFAT inhibitor FK506. ( F ) Change in CD8 + T cell proliferation and cytokine production in the presence or absence of NFAT inhibitor FK506. * P < 0.05; ** P < 0.01; *** P < 0.001; t test.

Article Snippet: Both wild-type human IL-2 and OMCPmutIL-2 were produced through transient transfection in CHO cell line (Celltheon) based on previously described methods ( ).

Techniques: Confocal Microscopy, In Vitro, Activation Assay, Generated, Expressing

( A ) Canonical pathway of NFAT activation through TCR signal transduction. ( B ) TCR signaling, as measured by Nur77 upregulation (representative FACS plot, left) in the presence of cytokines and variable concentrations of TCR agonistic antibody (anti-CD3) as well as 2 μg/mL of anti-CD28 (MFI, quantification from 5 individual Nur77GFP mice, right). ( C ) Relative gene expression of the TCR signaling pathway as defined by heatmap analysis in splenic murine CD8 + T cells cultured in the presence of anti-CD3/28 and various cytokines. ( D ) Phosphorylation of TCR signaling components of murine CD8 + T cells in the presence of wild-type IL-2 (blue), IL-15 (green), or OMCPmutIL-2 (red) or no cytokine (black) with anti-CD3/CD28 cross-linking antibodies. ( E ) Phosphorylation levels of CD3ζ and STAT-5 levels as measured by MFI in murine CD8 + T cells in the presence or absence of JAK1/3 inhibitor as compared with CD8 + T cells derived from Jak3 –/– mice. ( F ) Graphical representation of OMCPmutIL-2–mediated activation of NFAT activation at the expense of the canonical STAT5/AKT signaling pathways. ( G ) TCR signal transduction, as measured by Nur77 expression, in OT-1 clonotypic CD8 + T cells incubated with dendritic cells loaded with various SIINFEKL mutants with variable TCR binding avidity. * P < 0.05; ** P < 0.01; *** P < 0.001; t test.

Journal: JCI Insight

Article Title: A reengineered common chain cytokine augments CD8 + T cell–dependent immunotherapy

doi: 10.1172/jci.insight.158889

Figure Lengend Snippet: ( A ) Canonical pathway of NFAT activation through TCR signal transduction. ( B ) TCR signaling, as measured by Nur77 upregulation (representative FACS plot, left) in the presence of cytokines and variable concentrations of TCR agonistic antibody (anti-CD3) as well as 2 μg/mL of anti-CD28 (MFI, quantification from 5 individual Nur77GFP mice, right). ( C ) Relative gene expression of the TCR signaling pathway as defined by heatmap analysis in splenic murine CD8 + T cells cultured in the presence of anti-CD3/28 and various cytokines. ( D ) Phosphorylation of TCR signaling components of murine CD8 + T cells in the presence of wild-type IL-2 (blue), IL-15 (green), or OMCPmutIL-2 (red) or no cytokine (black) with anti-CD3/CD28 cross-linking antibodies. ( E ) Phosphorylation levels of CD3ζ and STAT-5 levels as measured by MFI in murine CD8 + T cells in the presence or absence of JAK1/3 inhibitor as compared with CD8 + T cells derived from Jak3 –/– mice. ( F ) Graphical representation of OMCPmutIL-2–mediated activation of NFAT activation at the expense of the canonical STAT5/AKT signaling pathways. ( G ) TCR signal transduction, as measured by Nur77 expression, in OT-1 clonotypic CD8 + T cells incubated with dendritic cells loaded with various SIINFEKL mutants with variable TCR binding avidity. * P < 0.05; ** P < 0.01; *** P < 0.001; t test.

Article Snippet: Both wild-type human IL-2 and OMCPmutIL-2 were produced through transient transfection in CHO cell line (Celltheon) based on previously described methods ( ).

Techniques: Activation Assay, Transduction, Expressing, Cell Culture, Derivative Assay, Incubation, Binding Assay

( A ) Time course analysis (0–60 minutes) of phosphorylation of CD3ζ and STAT5 in murine CD8 + T cells stimulated with OMCPmutIL-2 (red), wild-type IL-2 (blue), and IL-15 (green). ( B ) (Left) High-resolution confocal microscopy of human CD8 + T cell surface receptors IL-2Rβ (CD122) (green), CD3ζ (red), and NKG2D (pink) after 1 hour in the presence of plate-bound anti-CD3/28 with different cytokines. Visible colocalization of receptors is shown by arrows (yellow). Original magnification, ×63. (Right) Percentage of T cells demonstrating visible clustering of CD3ζ and IL-2Rβ per high-power field. n = 13. * P < 0.05; ** P < 0.01; *** P < 0.001; t test.

Journal: JCI Insight

Article Title: A reengineered common chain cytokine augments CD8 + T cell–dependent immunotherapy

doi: 10.1172/jci.insight.158889

Figure Lengend Snippet: ( A ) Time course analysis (0–60 minutes) of phosphorylation of CD3ζ and STAT5 in murine CD8 + T cells stimulated with OMCPmutIL-2 (red), wild-type IL-2 (blue), and IL-15 (green). ( B ) (Left) High-resolution confocal microscopy of human CD8 + T cell surface receptors IL-2Rβ (CD122) (green), CD3ζ (red), and NKG2D (pink) after 1 hour in the presence of plate-bound anti-CD3/28 with different cytokines. Visible colocalization of receptors is shown by arrows (yellow). Original magnification, ×63. (Right) Percentage of T cells demonstrating visible clustering of CD3ζ and IL-2Rβ per high-power field. n = 13. * P < 0.05; ** P < 0.01; *** P < 0.001; t test.

Article Snippet: Both wild-type human IL-2 and OMCPmutIL-2 were produced through transient transfection in CHO cell line (Celltheon) based on previously described methods ( ).

Techniques: Confocal Microscopy

( A ) High-resolution confocal microscopy of human CD8 + T cells evaluating receptor localization/clustering of CD3ζ (red) and IL-2Rβ/CD122 (pink) with lipid rafts (stained by Cholera Toxin B, CTB, in green). Clustering of receptors is shown by yellow arrow. ( B ) High-resolution confocal microscopy of human CD8 + T cell surface receptors (left panel) IL-2Rβ (CD122) (green), CD3ζ (red), and lipid rafts (stained by CTB in green) after lipid raft disruption by Methyl-β-cyclodextrin (MBCD) demonstrates no visible colocalization of receptors. Percentage clustering (right panel) shows little clustering and no difference between groups after MBCD treatment. Original magnification, ×63. ( C ) Flow cytometric analysis of CD3ζ and STAT5 phosphorylation after 1 hour of stimulation in various cytokines in the presence or absence of MBCD. ( D ) Phospho-CD3ζ and phospho-STAT5 expression in human PBL-derived CD8 + T cells after culture with OMCPmutIL-2 versus IL-2. ( E ) Phospho-CD3ζ and phospho-STAT5 expression in human PBL-derived CD8 + T cells after culture with mutIL-2–redirected constructs with different NKG2D ligands having different binding affinity. ** P < 0.01; t test ( B – D ) or ANOVA ( E ).

Journal: JCI Insight

Article Title: A reengineered common chain cytokine augments CD8 + T cell–dependent immunotherapy

doi: 10.1172/jci.insight.158889

Figure Lengend Snippet: ( A ) High-resolution confocal microscopy of human CD8 + T cells evaluating receptor localization/clustering of CD3ζ (red) and IL-2Rβ/CD122 (pink) with lipid rafts (stained by Cholera Toxin B, CTB, in green). Clustering of receptors is shown by yellow arrow. ( B ) High-resolution confocal microscopy of human CD8 + T cell surface receptors (left panel) IL-2Rβ (CD122) (green), CD3ζ (red), and lipid rafts (stained by CTB in green) after lipid raft disruption by Methyl-β-cyclodextrin (MBCD) demonstrates no visible colocalization of receptors. Percentage clustering (right panel) shows little clustering and no difference between groups after MBCD treatment. Original magnification, ×63. ( C ) Flow cytometric analysis of CD3ζ and STAT5 phosphorylation after 1 hour of stimulation in various cytokines in the presence or absence of MBCD. ( D ) Phospho-CD3ζ and phospho-STAT5 expression in human PBL-derived CD8 + T cells after culture with OMCPmutIL-2 versus IL-2. ( E ) Phospho-CD3ζ and phospho-STAT5 expression in human PBL-derived CD8 + T cells after culture with mutIL-2–redirected constructs with different NKG2D ligands having different binding affinity. ** P < 0.01; t test ( B – D ) or ANOVA ( E ).

Article Snippet: Both wild-type human IL-2 and OMCPmutIL-2 were produced through transient transfection in CHO cell line (Celltheon) based on previously described methods ( ).

Techniques: Confocal Microscopy, Staining, Expressing, Derivative Assay, Construct, Binding Assay

( A ) Quantification of mitochondria using high-resolution confocal microscopy using MitoTracker Deep Red dye (upper 2 panels) and electron microscopy (lower panel) depicting increased number of fused mitochondria in OMCPmutIL-2–treated CD8 + T cells. Original magnification, ×63 (middle panel) and ×1000 (lower panel). ( B ) Gene expression analysis showing increased NRF1 transcription factors in OMCPmutIL-2–expanded CD8 + T cells (upper panel). Flow cytometric analysis of mitochondrial membrane potential (middle) and oxygen consumption rate by Seahorse assay (lower) in murine CD8 + T cells expanded in IL-2 (blue), IL-15 (green), or OMCPmutIL-2 (red). ( C ) Analysis of differential expression of genes involved in oxidative phosphorylation as expressed by enrichment scores and heatmaps. ( D ) Flow cytometric quantification of PGC-1α and mitochondrial mass and Tcm after inhibition of PGC-1α. ( E ) PGC-1α levels, mitochondrial mass, and relative proportion of Tcm in the presence of constitutively active AKT (myrAKT mice) or pharmacologic AKT inhibition. ( F ) PD-1 expression as measured by MFI of murine CD8 + T cells in the presence of constitutively active AKT (myrAKT) or AKT inhibition. * P < 0.05; ** P < 0.01; *** P < 0.001; t test.

Journal: JCI Insight

Article Title: A reengineered common chain cytokine augments CD8 + T cell–dependent immunotherapy

doi: 10.1172/jci.insight.158889

Figure Lengend Snippet: ( A ) Quantification of mitochondria using high-resolution confocal microscopy using MitoTracker Deep Red dye (upper 2 panels) and electron microscopy (lower panel) depicting increased number of fused mitochondria in OMCPmutIL-2–treated CD8 + T cells. Original magnification, ×63 (middle panel) and ×1000 (lower panel). ( B ) Gene expression analysis showing increased NRF1 transcription factors in OMCPmutIL-2–expanded CD8 + T cells (upper panel). Flow cytometric analysis of mitochondrial membrane potential (middle) and oxygen consumption rate by Seahorse assay (lower) in murine CD8 + T cells expanded in IL-2 (blue), IL-15 (green), or OMCPmutIL-2 (red). ( C ) Analysis of differential expression of genes involved in oxidative phosphorylation as expressed by enrichment scores and heatmaps. ( D ) Flow cytometric quantification of PGC-1α and mitochondrial mass and Tcm after inhibition of PGC-1α. ( E ) PGC-1α levels, mitochondrial mass, and relative proportion of Tcm in the presence of constitutively active AKT (myrAKT mice) or pharmacologic AKT inhibition. ( F ) PD-1 expression as measured by MFI of murine CD8 + T cells in the presence of constitutively active AKT (myrAKT) or AKT inhibition. * P < 0.05; ** P < 0.01; *** P < 0.001; t test.

Article Snippet: Both wild-type human IL-2 and OMCPmutIL-2 were produced through transient transfection in CHO cell line (Celltheon) based on previously described methods ( ).

Techniques: Confocal Microscopy, Electron Microscopy, Expressing, Inhibition

( A ) In vitro cytotoxicity of anti-CD19 CAR T cells, expanded in various cytokines, against NALM6 CD19-expressing tumors. ( B ) Experimental design, tumor growth, and survival of B16 melanoma–bearing mice treated with adoptive transfer of pmel anti-GP100 TCR-transgenic CD8 + T cells expanded in the presence of IL-2 (blue), IL-15 (green), or OMCPmutIL-2 (red). ( C ) Experimental design, tumor growth, and survival of mice bearing CT26 colon cancer tumors. ( D ) Tumor growth and survival percentage of mice bearing tumor antigen ovalbumin expressing Lewis lung carcinoma (LLC ova ) in combinatorial immunotherapy with cytokines and checkpoint inhibitors CTLA-4 and PD-1. ( E ) Tumor growth in surviving mice after rechallenge with LLC ova . * P < 0.05; ** P < 0.01; *** P < 0.001; t test. s.q., subcutaneous.

Journal: JCI Insight

Article Title: A reengineered common chain cytokine augments CD8 + T cell–dependent immunotherapy

doi: 10.1172/jci.insight.158889

Figure Lengend Snippet: ( A ) In vitro cytotoxicity of anti-CD19 CAR T cells, expanded in various cytokines, against NALM6 CD19-expressing tumors. ( B ) Experimental design, tumor growth, and survival of B16 melanoma–bearing mice treated with adoptive transfer of pmel anti-GP100 TCR-transgenic CD8 + T cells expanded in the presence of IL-2 (blue), IL-15 (green), or OMCPmutIL-2 (red). ( C ) Experimental design, tumor growth, and survival of mice bearing CT26 colon cancer tumors. ( D ) Tumor growth and survival percentage of mice bearing tumor antigen ovalbumin expressing Lewis lung carcinoma (LLC ova ) in combinatorial immunotherapy with cytokines and checkpoint inhibitors CTLA-4 and PD-1. ( E ) Tumor growth in surviving mice after rechallenge with LLC ova . * P < 0.05; ** P < 0.01; *** P < 0.001; t test. s.q., subcutaneous.

Article Snippet: Both wild-type human IL-2 and OMCPmutIL-2 were produced through transient transfection in CHO cell line (Celltheon) based on previously described methods ( ).

Techniques: In Vitro, Expressing, Adoptive Transfer Assay, Transgenic Assay

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1) Product Images from "Retargeting Interleukin-2 Signaling to NKG2D-Expressing Tumor Infiltrating Leukocytes Improves Adoptive Transfer Immunotherapy"

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