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tlr9  (MedChemExpress)


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    MedChemExpress tlr9
    Reduced frequency yet heightened cytotoxicity of peripheral blood NK cells in SLE patients. (a) Representative flow cytometry plots depicting gating strategy for TBNK cell populations. (b) Quantitative analysis of TBNK subpopulations in SLE patients ( n = 54) versus healthy controls (HCs; n = 43). (c) Correlation of peripheral blood NK cell percentage and SLEDAI score in SLE patients. (d) Intracellular expression of Granzyme B and TNF‐α in primary human NK cells following stimulation with PMA (10 ng/mL), ionomycin (1 µg/mL) and brefeldin A (BFA; 1 µg/mL) for 12 h, analysed by flow cytometry. (e) Quantification of granzyme B and TNF‐α expression. (f) Serum concentration of IL‐6, IL‐17A and TNF‐α in the serum of HC and SLE ( n = 12). (g) The cytotoxicity of NK against K‐562 cells at varying effector: target cell ratios. NK cells were purified from PBMC. NK cells and target cells were co‐cultured with tumour cells for 4 h. (h) Correlation between NK cell percentage and SLEDAI score in SLE patients ( n = 12). (i) Correlation of NK cell cytotoxicity with Streptococcus anginosus abundance in SLE patients ( n = 12). (j) Surface expression of TLR2, TLR4, TLR6, TLR7 and <t>TLR9</t> on human NK cells. (k) Quantitative analysis of TLR receptor mean fluorescence intensity (MFI) on NK cells ( n = 6). Data are shown as mean ± SD, with individual data points representing biological replicates (average of technical duplicates). Statistical comparisons were performed using one‐way ANOVA with Tukey post‐tests. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. ns indicates not significant.
    Tlr9, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    tlr9 - by Bioz Stars, 2026-02
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    Images

    1) Product Images from "Extracellular Vesicles Derived From Streptococcus anginosus Aggravate Lupus Nephritis by Triggering TLR2‐MyD88‐NF‐κB Signalling in NK Cells"

    Article Title: Extracellular Vesicles Derived From Streptococcus anginosus Aggravate Lupus Nephritis by Triggering TLR2‐MyD88‐NF‐κB Signalling in NK Cells

    Journal: Journal of Extracellular Vesicles

    doi: 10.1002/jev2.70134

    Reduced frequency yet heightened cytotoxicity of peripheral blood NK cells in SLE patients. (a) Representative flow cytometry plots depicting gating strategy for TBNK cell populations. (b) Quantitative analysis of TBNK subpopulations in SLE patients ( n = 54) versus healthy controls (HCs; n = 43). (c) Correlation of peripheral blood NK cell percentage and SLEDAI score in SLE patients. (d) Intracellular expression of Granzyme B and TNF‐α in primary human NK cells following stimulation with PMA (10 ng/mL), ionomycin (1 µg/mL) and brefeldin A (BFA; 1 µg/mL) for 12 h, analysed by flow cytometry. (e) Quantification of granzyme B and TNF‐α expression. (f) Serum concentration of IL‐6, IL‐17A and TNF‐α in the serum of HC and SLE ( n = 12). (g) The cytotoxicity of NK against K‐562 cells at varying effector: target cell ratios. NK cells were purified from PBMC. NK cells and target cells were co‐cultured with tumour cells for 4 h. (h) Correlation between NK cell percentage and SLEDAI score in SLE patients ( n = 12). (i) Correlation of NK cell cytotoxicity with Streptococcus anginosus abundance in SLE patients ( n = 12). (j) Surface expression of TLR2, TLR4, TLR6, TLR7 and TLR9 on human NK cells. (k) Quantitative analysis of TLR receptor mean fluorescence intensity (MFI) on NK cells ( n = 6). Data are shown as mean ± SD, with individual data points representing biological replicates (average of technical duplicates). Statistical comparisons were performed using one‐way ANOVA with Tukey post‐tests. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. ns indicates not significant.
    Figure Legend Snippet: Reduced frequency yet heightened cytotoxicity of peripheral blood NK cells in SLE patients. (a) Representative flow cytometry plots depicting gating strategy for TBNK cell populations. (b) Quantitative analysis of TBNK subpopulations in SLE patients ( n = 54) versus healthy controls (HCs; n = 43). (c) Correlation of peripheral blood NK cell percentage and SLEDAI score in SLE patients. (d) Intracellular expression of Granzyme B and TNF‐α in primary human NK cells following stimulation with PMA (10 ng/mL), ionomycin (1 µg/mL) and brefeldin A (BFA; 1 µg/mL) for 12 h, analysed by flow cytometry. (e) Quantification of granzyme B and TNF‐α expression. (f) Serum concentration of IL‐6, IL‐17A and TNF‐α in the serum of HC and SLE ( n = 12). (g) The cytotoxicity of NK against K‐562 cells at varying effector: target cell ratios. NK cells were purified from PBMC. NK cells and target cells were co‐cultured with tumour cells for 4 h. (h) Correlation between NK cell percentage and SLEDAI score in SLE patients ( n = 12). (i) Correlation of NK cell cytotoxicity with Streptococcus anginosus abundance in SLE patients ( n = 12). (j) Surface expression of TLR2, TLR4, TLR6, TLR7 and TLR9 on human NK cells. (k) Quantitative analysis of TLR receptor mean fluorescence intensity (MFI) on NK cells ( n = 6). Data are shown as mean ± SD, with individual data points representing biological replicates (average of technical duplicates). Statistical comparisons were performed using one‐way ANOVA with Tukey post‐tests. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. ns indicates not significant.

    Techniques Used: Flow Cytometry, Expressing, Concentration Assay, Purification, Cell Culture, Fluorescence



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    Reduced frequency yet heightened cytotoxicity of peripheral blood NK cells in SLE patients. (a) Representative flow cytometry plots depicting gating strategy for TBNK cell populations. (b) Quantitative analysis of TBNK subpopulations in SLE patients ( n = 54) versus healthy controls (HCs; n = 43). (c) Correlation of peripheral blood NK cell percentage and SLEDAI score in SLE patients. (d) Intracellular expression of Granzyme B and TNF‐α in primary human NK cells following stimulation with PMA (10 ng/mL), ionomycin (1 µg/mL) and brefeldin A (BFA; 1 µg/mL) for 12 h, analysed by flow cytometry. (e) Quantification of granzyme B and TNF‐α expression. (f) Serum concentration of IL‐6, IL‐17A and TNF‐α in the serum of HC and SLE ( n = 12). (g) The cytotoxicity of NK against K‐562 cells at varying effector: target cell ratios. NK cells were purified from PBMC. NK cells and target cells were co‐cultured with tumour cells for 4 h. (h) Correlation between NK cell percentage and SLEDAI score in SLE patients ( n = 12). (i) Correlation of NK cell cytotoxicity with Streptococcus anginosus abundance in SLE patients ( n = 12). (j) Surface expression of TLR2, TLR4, TLR6, TLR7 and <t>TLR9</t> on human NK cells. (k) Quantitative analysis of TLR receptor mean fluorescence intensity (MFI) on NK cells ( n = 6). Data are shown as mean ± SD, with individual data points representing biological replicates (average of technical duplicates). Statistical comparisons were performed using one‐way ANOVA with Tukey post‐tests. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. ns indicates not significant.
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    Reduced frequency yet heightened cytotoxicity of peripheral blood NK cells in SLE patients. (a) Representative flow cytometry plots depicting gating strategy for TBNK cell populations. (b) Quantitative analysis of TBNK subpopulations in SLE patients ( n = 54) versus healthy controls (HCs; n = 43). (c) Correlation of peripheral blood NK cell percentage and SLEDAI score in SLE patients. (d) Intracellular expression of Granzyme B and TNF‐α in primary human NK cells following stimulation with PMA (10 ng/mL), ionomycin (1 µg/mL) and brefeldin A (BFA; 1 µg/mL) for 12 h, analysed by flow cytometry. (e) Quantification of granzyme B and TNF‐α expression. (f) Serum concentration of IL‐6, IL‐17A and TNF‐α in the serum of HC and SLE ( n = 12). (g) The cytotoxicity of NK against K‐562 cells at varying effector: target cell ratios. NK cells were purified from PBMC. NK cells and target cells were co‐cultured with tumour cells for 4 h. (h) Correlation between NK cell percentage and SLEDAI score in SLE patients ( n = 12). (i) Correlation of NK cell cytotoxicity with Streptococcus anginosus abundance in SLE patients ( n = 12). (j) Surface expression of TLR2, TLR4, TLR6, TLR7 and <t>TLR9</t> on human NK cells. (k) Quantitative analysis of TLR receptor mean fluorescence intensity (MFI) on NK cells ( n = 6). Data are shown as mean ± SD, with individual data points representing biological replicates (average of technical duplicates). Statistical comparisons were performed using one‐way ANOVA with Tukey post‐tests. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. ns indicates not significant.
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    Reduced frequency yet heightened cytotoxicity of peripheral blood NK cells in SLE patients. (a) Representative flow cytometry plots depicting gating strategy for TBNK cell populations. (b) Quantitative analysis of TBNK subpopulations in SLE patients ( n = 54) versus healthy controls (HCs; n = 43). (c) Correlation of peripheral blood NK cell percentage and SLEDAI score in SLE patients. (d) Intracellular expression of Granzyme B and TNF‐α in primary human NK cells following stimulation with PMA (10 ng/mL), ionomycin (1 µg/mL) and brefeldin A (BFA; 1 µg/mL) for 12 h, analysed by flow cytometry. (e) Quantification of granzyme B and TNF‐α expression. (f) Serum concentration of IL‐6, IL‐17A and TNF‐α in the serum of HC and SLE ( n = 12). (g) The cytotoxicity of NK against K‐562 cells at varying effector: target cell ratios. NK cells were purified from PBMC. NK cells and target cells were co‐cultured with tumour cells for 4 h. (h) Correlation between NK cell percentage and SLEDAI score in SLE patients ( n = 12). (i) Correlation of NK cell cytotoxicity with Streptococcus anginosus abundance in SLE patients ( n = 12). (j) Surface expression of TLR2, TLR4, TLR6, TLR7 and TLR9 on human NK cells. (k) Quantitative analysis of TLR receptor mean fluorescence intensity (MFI) on NK cells ( n = 6). Data are shown as mean ± SD, with individual data points representing biological replicates (average of technical duplicates). Statistical comparisons were performed using one‐way ANOVA with Tukey post‐tests. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. ns indicates not significant.

    Journal: Journal of Extracellular Vesicles

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    doi: 10.1002/jev2.70134

    Figure Lengend Snippet: Reduced frequency yet heightened cytotoxicity of peripheral blood NK cells in SLE patients. (a) Representative flow cytometry plots depicting gating strategy for TBNK cell populations. (b) Quantitative analysis of TBNK subpopulations in SLE patients ( n = 54) versus healthy controls (HCs; n = 43). (c) Correlation of peripheral blood NK cell percentage and SLEDAI score in SLE patients. (d) Intracellular expression of Granzyme B and TNF‐α in primary human NK cells following stimulation with PMA (10 ng/mL), ionomycin (1 µg/mL) and brefeldin A (BFA; 1 µg/mL) for 12 h, analysed by flow cytometry. (e) Quantification of granzyme B and TNF‐α expression. (f) Serum concentration of IL‐6, IL‐17A and TNF‐α in the serum of HC and SLE ( n = 12). (g) The cytotoxicity of NK against K‐562 cells at varying effector: target cell ratios. NK cells were purified from PBMC. NK cells and target cells were co‐cultured with tumour cells for 4 h. (h) Correlation between NK cell percentage and SLEDAI score in SLE patients ( n = 12). (i) Correlation of NK cell cytotoxicity with Streptococcus anginosus abundance in SLE patients ( n = 12). (j) Surface expression of TLR2, TLR4, TLR6, TLR7 and TLR9 on human NK cells. (k) Quantitative analysis of TLR receptor mean fluorescence intensity (MFI) on NK cells ( n = 6). Data are shown as mean ± SD, with individual data points representing biological replicates (average of technical duplicates). Statistical comparisons were performed using one‐way ANOVA with Tukey post‐tests. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. ns indicates not significant.

    Article Snippet: TLR2 inhibitor (C29, Cat: HY‐100461), TLR4 (Stepharine, HY‐N9347), TLR7 (Enpatoran, HY‐134581A), TLR9 (AT791, HY‐124603) and MyD88 inhibitor (MyD88‐IN‐1, Cat: HY‐149992) were obtained from MedChemExpress (MCE, USA).

    Techniques: Flow Cytometry, Expressing, Concentration Assay, Purification, Cell Culture, Fluorescence