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easyseptm direct human neutrophil isolation kit (STEMCELL Technologies Inc)

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STEMCELL Technologies Inc easyseptm direct human neutrophil isolation kit
Easyseptm Direct Human Neutrophil Isolation Kit, supplied by STEMCELL Technologies Inc, 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

easyseptm direct human neutrophil isolation kit - by Bioz Stars, 2026-03

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Ex vivo expansion and pharmacological modulation of NK cell viability and phenotype. ( A ) Representative flow cytometer density plots of CD3 versus CD56 expression in cell preparations at days 0, 7, and 14 of the expansion protocol. ( B ) Distribution of viable cells into four CD3/CD56 subsets: CD3⁻CD56 + (blue), CD3 + CD56 + (green), CD3 + CD56⁻ (dark gray), and CD3⁻CD56⁻ (light gray). ( C ) Percentage of viable NK cells at days 0, 7, and 14, determined by live/dead staining (live = green; dead = blue). ( D , E ) Dose–response curves for expanded NK cell viability, treated with increasing concentrations of propranolol (D) and rapamycin (E) for 48 h. ( F ) Representative flow cytometry plot of freshly isolated NK cells. ( G ) Comparison of NK cells phenotypes after isolation versus 14 days of expansion. Data are presented as mean ± SEM for n = 4–5 independent donors. CD, cluster of differentiation; KLRG1, killer cell lectin-like receptor subfamily G member 1; LAG-3, lymphocyte-activation gene 3; NK, natural killer; NKG2A, natural killer group 2, member A; NKG2D, natural killer group 2, member D; PD-1, programmed death-1.

Journal: Scientific Reports

Article Title: Natural killer cells from endurance-trained older adults show improved functional and metabolic responses to adrenergic blockade and mTOR inhibition

doi: 10.1038/s41598-025-06057-y

Figure Lengend Snippet: Ex vivo expansion and pharmacological modulation of NK cell viability and phenotype. ( A ) Representative flow cytometer density plots of CD3 versus CD56 expression in cell preparations at days 0, 7, and 14 of the expansion protocol. ( B ) Distribution of viable cells into four CD3/CD56 subsets: CD3⁻CD56 + (blue), CD3 + CD56 + (green), CD3 + CD56⁻ (dark gray), and CD3⁻CD56⁻ (light gray). ( C ) Percentage of viable NK cells at days 0, 7, and 14, determined by live/dead staining (live = green; dead = blue). ( D , E ) Dose–response curves for expanded NK cell viability, treated with increasing concentrations of propranolol (D) and rapamycin (E) for 48 h. ( F ) Representative flow cytometry plot of freshly isolated NK cells. ( G ) Comparison of NK cells phenotypes after isolation versus 14 days of expansion. Data are presented as mean ± SEM for n = 4–5 independent donors. CD, cluster of differentiation; KLRG1, killer cell lectin-like receptor subfamily G member 1; LAG-3, lymphocyte-activation gene 3; NK, natural killer; NKG2A, natural killer group 2, member A; NKG2D, natural killer group 2, member D; PD-1, programmed death-1.

Article Snippet: We isolated NK cells from whole blood in both groups using the EasySepTM Direct Human NK cell isolation kit (STEMCELL Technologies, Vancouver, CA).

Techniques: Ex Vivo, Flow Cytometry, Expressing, Staining, Isolation, Comparison, Activation Assay

Propranolol dose-response effects on NK cells phenotype, activation, and regulatory receptor expression. Expanded NK cells were treated with increasing concentrations of propranolol (0, 10, 20, 50, 100, or 200 ng/mL) in the absence or presence of an inflammatory stimulus (PMA plus ionomycin, brefeldin A, and monensin). ( A ) Total NK cells (CD3⁻CD56 + ). ( B , C ) Cytotoxic (CD56 dim CD16 bright ) and effector (CD56 bright CD16 dim ) subset. ( D – F ) Activation (CD38), differentiation (CD57), and degranulation (CD107a) markers. ( G ) Senescence marker KLRG1. ( H – J ) Regulatory receptors LAG-3, NKG2A, and NKG2D. ( K – L ) Immune-exhaustion markers PD-1 and TIM-3. Data are presented as mean ± SEM from n = 4 untrained and n = 5 endurance-trained donors. * P < 0.05 versus untreated control; & P < 0.05 versus PMA; # P < 0.05 between PMA-stimulated and unstimulated at the same dose. All comparisons were determined using Bonferroni post hoc tests following a significant interaction effect detected by two-way ANOVA. CD, cluster of differentiation; KLRG1, killer cell lectin-like receptor subfamily G member 1; LAG-3, lymphocyte-activation gene 3; NK, natural killer; NKG2A, natural killer group 2, member A; NKG2D, natural killer group 2, member D; PD-1, programmed death-1; PMA, phorbol 12-myristate 13-acetate; TIM-3, T-cell immunoglobulin and mucin-domain containing-3.

Journal: Scientific Reports

Article Title: Natural killer cells from endurance-trained older adults show improved functional and metabolic responses to adrenergic blockade and mTOR inhibition

doi: 10.1038/s41598-025-06057-y

Figure Lengend Snippet: Propranolol dose-response effects on NK cells phenotype, activation, and regulatory receptor expression. Expanded NK cells were treated with increasing concentrations of propranolol (0, 10, 20, 50, 100, or 200 ng/mL) in the absence or presence of an inflammatory stimulus (PMA plus ionomycin, brefeldin A, and monensin). ( A ) Total NK cells (CD3⁻CD56 + ). ( B , C ) Cytotoxic (CD56 dim CD16 bright ) and effector (CD56 bright CD16 dim ) subset. ( D – F ) Activation (CD38), differentiation (CD57), and degranulation (CD107a) markers. ( G ) Senescence marker KLRG1. ( H – J ) Regulatory receptors LAG-3, NKG2A, and NKG2D. ( K – L ) Immune-exhaustion markers PD-1 and TIM-3. Data are presented as mean ± SEM from n = 4 untrained and n = 5 endurance-trained donors. * P < 0.05 versus untreated control; & P < 0.05 versus PMA; # P < 0.05 between PMA-stimulated and unstimulated at the same dose. All comparisons were determined using Bonferroni post hoc tests following a significant interaction effect detected by two-way ANOVA. CD, cluster of differentiation; KLRG1, killer cell lectin-like receptor subfamily G member 1; LAG-3, lymphocyte-activation gene 3; NK, natural killer; NKG2A, natural killer group 2, member A; NKG2D, natural killer group 2, member D; PD-1, programmed death-1; PMA, phorbol 12-myristate 13-acetate; TIM-3, T-cell immunoglobulin and mucin-domain containing-3.

Article Snippet: We isolated NK cells from whole blood in both groups using the EasySepTM Direct Human NK cell isolation kit (STEMCELL Technologies, Vancouver, CA).

Techniques: Activation Assay, Expressing, Marker, Control

Differential effects of propranolol and inflammatory stimulation on NK-cell phenotype in untrained versus trained groups. Expanded NK cells were treated with propranolol (50 or 100 ng/mL) in the absence or presence of an inflammatory cocktail (PMA/ionomycin with brefeldin A and monensin). ( A ) Total NK cells (CD3⁻CD56 + ). ( B , C ) Cytotoxic (CD56 dim CD16 bright ) and effector (CD56 bright CD16 dim ) subset frequencies. ( D – F ) Expression of activation (CD38), differentiation (CD57), and degranulation (CD107a) markers. ( G ) Senescence marker KLRG1. ( H – J ) Regulatory receptors LAG-3, NKG2A, and NKG2D. ( K , L ) Immune-exhaustion markers PD-1 and TIM-3. Data are presented as mean ± SEM from n = 4–5 donors per group. * P < 0.05 versus untreated control; # P < 0.05 between untrained and trained at the same concentration (Bonferroni post hoc test following a significant interaction effect in two-way ANOVA). CD, cluster of differentiation; KLRG1, killer cell lectin-like receptor subfamily G member 1; LAG-3, lymphocyte-activation gene 3; NK, natural killer; NKG2A, natural killer group 2, member A; NKG2D, natural killer group 2, member D; PD-1, programmed death-1; PMA, phorbol 12-myristate 13-acetate; TIM-3, T-cell immunoglobulin and mucin-domain containing-3.

Journal: Scientific Reports

Article Title: Natural killer cells from endurance-trained older adults show improved functional and metabolic responses to adrenergic blockade and mTOR inhibition

doi: 10.1038/s41598-025-06057-y

Figure Lengend Snippet: Differential effects of propranolol and inflammatory stimulation on NK-cell phenotype in untrained versus trained groups. Expanded NK cells were treated with propranolol (50 or 100 ng/mL) in the absence or presence of an inflammatory cocktail (PMA/ionomycin with brefeldin A and monensin). ( A ) Total NK cells (CD3⁻CD56 + ). ( B , C ) Cytotoxic (CD56 dim CD16 bright ) and effector (CD56 bright CD16 dim ) subset frequencies. ( D – F ) Expression of activation (CD38), differentiation (CD57), and degranulation (CD107a) markers. ( G ) Senescence marker KLRG1. ( H – J ) Regulatory receptors LAG-3, NKG2A, and NKG2D. ( K , L ) Immune-exhaustion markers PD-1 and TIM-3. Data are presented as mean ± SEM from n = 4–5 donors per group. * P < 0.05 versus untreated control; # P < 0.05 between untrained and trained at the same concentration (Bonferroni post hoc test following a significant interaction effect in two-way ANOVA). CD, cluster of differentiation; KLRG1, killer cell lectin-like receptor subfamily G member 1; LAG-3, lymphocyte-activation gene 3; NK, natural killer; NKG2A, natural killer group 2, member A; NKG2D, natural killer group 2, member D; PD-1, programmed death-1; PMA, phorbol 12-myristate 13-acetate; TIM-3, T-cell immunoglobulin and mucin-domain containing-3.

Article Snippet: We isolated NK cells from whole blood in both groups using the EasySepTM Direct Human NK cell isolation kit (STEMCELL Technologies, Vancouver, CA).

Techniques: Expressing, Activation Assay, Marker, Control, Concentration Assay

Dose-response effects of rapamycin on NK cells phenotype, activation, and regulatory receptor expression. NK cells expanded for 14 days were treated with increasing concentrations of rapamycin (0, 10, 25, 50, or 100 ng/mL) in the absence or presence of an inflammatory stimulus (PMA, ionomycin, brefeldin A, and monensin). ( A ) Total NK cells (CD3⁻CD56 + ). ( B , C ) Cytotoxic (CD56 dim CD16 bright ) and effector (CD56 bright CD16 dim ) subset. ( D – F ) Expression of activation (CD38), differentiation (CD57), and degranulation (CD107a) markers. ( G ) Senescence marker KLRG1. ( H – J ) Regulatory receptors LAG-3, NKG2A, and NKG2D. ( K , L ) Immune-exhaustion markers PD-1 and TIM-3. Data are presented as mean ± SEM from n = 4 untrained and n = 5 endurance-trained donors. * P < 0.05 versus untreated control; & P < 0.05 versus PMA; # P < 0.05 between PMA-stimulated and unstimulated at the same dose. All comparisons were determined using Bonferroni post hoc tests following a significant interaction effect detected by two-way ANOVA. CD, cluster of differentiation; KLRG1, killer cell lectin-like receptor subfamily G member 1; LAG-3, lymphocyte-activation gene 3; NK, natural killer; NKG2A, natural killer group 2, member A; NKG2D, natural killer group 2, member D; PD-1, programmed death-1; PMA, phorbol 12-myristate 13-acetate; TIM-3, T-cell immunoglobulin and mucin-domain containing-3.

Journal: Scientific Reports

Article Title: Natural killer cells from endurance-trained older adults show improved functional and metabolic responses to adrenergic blockade and mTOR inhibition

doi: 10.1038/s41598-025-06057-y

Figure Lengend Snippet: Dose-response effects of rapamycin on NK cells phenotype, activation, and regulatory receptor expression. NK cells expanded for 14 days were treated with increasing concentrations of rapamycin (0, 10, 25, 50, or 100 ng/mL) in the absence or presence of an inflammatory stimulus (PMA, ionomycin, brefeldin A, and monensin). ( A ) Total NK cells (CD3⁻CD56 + ). ( B , C ) Cytotoxic (CD56 dim CD16 bright ) and effector (CD56 bright CD16 dim ) subset. ( D – F ) Expression of activation (CD38), differentiation (CD57), and degranulation (CD107a) markers. ( G ) Senescence marker KLRG1. ( H – J ) Regulatory receptors LAG-3, NKG2A, and NKG2D. ( K , L ) Immune-exhaustion markers PD-1 and TIM-3. Data are presented as mean ± SEM from n = 4 untrained and n = 5 endurance-trained donors. * P < 0.05 versus untreated control; & P < 0.05 versus PMA; # P < 0.05 between PMA-stimulated and unstimulated at the same dose. All comparisons were determined using Bonferroni post hoc tests following a significant interaction effect detected by two-way ANOVA. CD, cluster of differentiation; KLRG1, killer cell lectin-like receptor subfamily G member 1; LAG-3, lymphocyte-activation gene 3; NK, natural killer; NKG2A, natural killer group 2, member A; NKG2D, natural killer group 2, member D; PD-1, programmed death-1; PMA, phorbol 12-myristate 13-acetate; TIM-3, T-cell immunoglobulin and mucin-domain containing-3.

Article Snippet: We isolated NK cells from whole blood in both groups using the EasySepTM Direct Human NK cell isolation kit (STEMCELL Technologies, Vancouver, CA).

Techniques: Activation Assay, Expressing, Marker, Control

Differential effects of propranolol and inflammatory stimulation on NK-cell phenotype in untrained versus trained older adults. Expanded NK cells were treated with rapamycin (10 or 100 ng/mL) in the absence or presence of an inflammatory cocktail (PMA/ionomycin with brefeldin A and monensin). ( A ) Total NK cells (CD3⁻CD56 + ). ( B , C ) Cytotoxic (CD56 dim CD16 bright ) and effector (CD56 bright CD16 dim ) subset frequencies. ( D – F ) Expression of activation (CD38), differentiation (CD57), and degranulation (CD107a) markers. ( G ) Senescence marker KLRG1. ( H – J ) Regulatory receptors LAG-3, NKG2A, and NKG2D. ( K – L ) Immune-exhaustion markers PD-1 and TIM-3. Data are presented as mean ± SEM from n = 4–5 donors per group. * P < 0.05 versus untreated control; # P < 0.05 between untrained and trained at the same concentration (Bonferroni post hoc test following a significant interaction effect in two-way ANOVA). CD, cluster of differentiation; KLRG1, killer cell lectin-like receptor subfamily G member 1; LAG-3, lymphocyte-activation gene 3; NK, natural killer; NKG2A, natural killer group 2, member A; NKG2D, natural killer group 2, member D; PD-1, programmed death-1; PMA, phorbol 12-myristate 13-acetate; TIM-3, T-cell immunoglobulin and mucin-domain containing-3.

Journal: Scientific Reports

Article Title: Natural killer cells from endurance-trained older adults show improved functional and metabolic responses to adrenergic blockade and mTOR inhibition

doi: 10.1038/s41598-025-06057-y

Figure Lengend Snippet: Differential effects of propranolol and inflammatory stimulation on NK-cell phenotype in untrained versus trained older adults. Expanded NK cells were treated with rapamycin (10 or 100 ng/mL) in the absence or presence of an inflammatory cocktail (PMA/ionomycin with brefeldin A and monensin). ( A ) Total NK cells (CD3⁻CD56 + ). ( B , C ) Cytotoxic (CD56 dim CD16 bright ) and effector (CD56 bright CD16 dim ) subset frequencies. ( D – F ) Expression of activation (CD38), differentiation (CD57), and degranulation (CD107a) markers. ( G ) Senescence marker KLRG1. ( H – J ) Regulatory receptors LAG-3, NKG2A, and NKG2D. ( K – L ) Immune-exhaustion markers PD-1 and TIM-3. Data are presented as mean ± SEM from n = 4–5 donors per group. * P < 0.05 versus untreated control; # P < 0.05 between untrained and trained at the same concentration (Bonferroni post hoc test following a significant interaction effect in two-way ANOVA). CD, cluster of differentiation; KLRG1, killer cell lectin-like receptor subfamily G member 1; LAG-3, lymphocyte-activation gene 3; NK, natural killer; NKG2A, natural killer group 2, member A; NKG2D, natural killer group 2, member D; PD-1, programmed death-1; PMA, phorbol 12-myristate 13-acetate; TIM-3, T-cell immunoglobulin and mucin-domain containing-3.

Article Snippet: We isolated NK cells from whole blood in both groups using the EasySepTM Direct Human NK cell isolation kit (STEMCELL Technologies, Vancouver, CA).

Techniques: Expressing, Activation Assay, Marker, Control, Concentration Assay

Enhanced oxidative metabolism in NK cells from trained versus untrained older adults. ( A ) Frequency of isolated NK cells (CD3⁻CD56 + ) in peripheral blood. ( B , C ) Representative Seahorse metabolic flux traces showing OCR and ECAR for NK cells from untrained (blue circles) and endurance-trained (green squares) donors. ( D ) Basal OCR. ( E ) Maximal OCR, measured after FCCP injection. ( F ) Spare respiratory capacity (maximal OCR – basal OCR). ( G ) Maximal ECAR. ( H ) OCR/ECAR ratio, indicating relative reliance on oxidative versus glycolytic metabolism. ( I ) ATP-linked OCR (basal OCR – oligomycin-inhibited OCR). ( J ) Proton leak (oligomycin‐inhibited OCR – non-mitochondrial respiration). Data are presented as mean ± SEM from n = 4 untrained and n = 5 endurance-trained donors. * P < 0.05 versus untreated control (Mann-Whitney U test). OCR, oxygen‐consumption rate; ECAR, extracellular acidification rate; FCCP, carbonyl cyanide-p-trifluoromethoxyphenylhydrazone.

Journal: Scientific Reports

Article Title: Natural killer cells from endurance-trained older adults show improved functional and metabolic responses to adrenergic blockade and mTOR inhibition

doi: 10.1038/s41598-025-06057-y

Figure Lengend Snippet: Enhanced oxidative metabolism in NK cells from trained versus untrained older adults. ( A ) Frequency of isolated NK cells (CD3⁻CD56 + ) in peripheral blood. ( B , C ) Representative Seahorse metabolic flux traces showing OCR and ECAR for NK cells from untrained (blue circles) and endurance-trained (green squares) donors. ( D ) Basal OCR. ( E ) Maximal OCR, measured after FCCP injection. ( F ) Spare respiratory capacity (maximal OCR – basal OCR). ( G ) Maximal ECAR. ( H ) OCR/ECAR ratio, indicating relative reliance on oxidative versus glycolytic metabolism. ( I ) ATP-linked OCR (basal OCR – oligomycin-inhibited OCR). ( J ) Proton leak (oligomycin‐inhibited OCR – non-mitochondrial respiration). Data are presented as mean ± SEM from n = 4 untrained and n = 5 endurance-trained donors. * P < 0.05 versus untreated control (Mann-Whitney U test). OCR, oxygen‐consumption rate; ECAR, extracellular acidification rate; FCCP, carbonyl cyanide-p-trifluoromethoxyphenylhydrazone.

Article Snippet: We isolated NK cells from whole blood in both groups using the EasySepTM Direct Human NK cell isolation kit (STEMCELL Technologies, Vancouver, CA).

Techniques: Isolation, Injection, Control, MANN-WHITNEY

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