control peptide Search Results


90
Rockland Immunochemicals p29ing4
Figure 1: Expression of p33ING1b and <t>p29ING4</t> in renal cell carcinoma. (a) mRNA expression of p33ING1b and p29ING4 was increased at early and late stages of disease with higher expression of both genes at late stages of disease compared to early stages (Robson stages III/IV vs. I/II) (p33ING1b and p29ING4: stages I/II and III/IV vs. normal tissue p<0.001 and p<0.0001, respectively; p33ING1b and p29ING4: stages III/IV vs. I/II p<0.01 and p<0.001, respectively). (b) Results of the real time RT-PCR were normalized to kidney normal tissue and expressed as x-fold difference (2- ∆∆Ct). Expression of p33ING1b and p29ING4 by renal carcinoma cells was confirmed (Cy3 red; DAPI blue (nuclear counterstaining)). (c) Sections are representative of n=30 patients/group. Representative western blots of p33ING1b and p29ING4 (loading control ß-actin).
P29ing4, supplied by Rockland Immunochemicals, 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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93
Rockland Immunochemicals rhodamine
Figure 1: Expression of p33ING1b and <t>p29ING4</t> in renal cell carcinoma. (a) mRNA expression of p33ING1b and p29ING4 was increased at early and late stages of disease with higher expression of both genes at late stages of disease compared to early stages (Robson stages III/IV vs. I/II) (p33ING1b and p29ING4: stages I/II and III/IV vs. normal tissue p<0.001 and p<0.0001, respectively; p33ING1b and p29ING4: stages III/IV vs. I/II p<0.01 and p<0.001, respectively). (b) Results of the real time RT-PCR were normalized to kidney normal tissue and expressed as x-fold difference (2- ∆∆Ct). Expression of p33ING1b and p29ING4 by renal carcinoma cells was confirmed (Cy3 red; DAPI blue (nuclear counterstaining)). (c) Sections are representative of n=30 patients/group. Representative western blots of p33ING1b and p29ING4 (loading control ß-actin).
Rhodamine, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 1 article reviews
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85
Rockland Immunochemicals histone h3
Figure 1: Expression of p33ING1b and <t>p29ING4</t> in renal cell carcinoma. (a) mRNA expression of p33ING1b and p29ING4 was increased at early and late stages of disease with higher expression of both genes at late stages of disease compared to early stages (Robson stages III/IV vs. I/II) (p33ING1b and p29ING4: stages I/II and III/IV vs. normal tissue p<0.001 and p<0.0001, respectively; p33ING1b and p29ING4: stages III/IV vs. I/II p<0.01 and p<0.001, respectively). (b) Results of the real time RT-PCR were normalized to kidney normal tissue and expressed as x-fold difference (2- ∆∆Ct). Expression of p33ING1b and p29ING4 by renal carcinoma cells was confirmed (Cy3 red; DAPI blue (nuclear counterstaining)). (c) Sections are representative of n=30 patients/group. Representative western blots of p33ING1b and p29ING4 (loading control ß-actin).
Histone H3, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 85 stars, based on 1 article reviews
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96
Cellular Technology Ltd cef peptide pool
Figure 1: Expression of p33ING1b and <t>p29ING4</t> in renal cell carcinoma. (a) mRNA expression of p33ING1b and p29ING4 was increased at early and late stages of disease with higher expression of both genes at late stages of disease compared to early stages (Robson stages III/IV vs. I/II) (p33ING1b and p29ING4: stages I/II and III/IV vs. normal tissue p<0.001 and p<0.0001, respectively; p33ING1b and p29ING4: stages III/IV vs. I/II p<0.01 and p<0.001, respectively). (b) Results of the real time RT-PCR were normalized to kidney normal tissue and expressed as x-fold difference (2- ∆∆Ct). Expression of p33ING1b and p29ING4 by renal carcinoma cells was confirmed (Cy3 red; DAPI blue (nuclear counterstaining)). (c) Sections are representative of n=30 patients/group. Representative western blots of p33ING1b and p29ING4 (loading control ß-actin).
Cef Peptide Pool, supplied by Cellular Technology Ltd, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 1 article reviews
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93
Novus Biologicals peptide
Figure 1: Expression of p33ING1b and <t>p29ING4</t> in renal cell carcinoma. (a) mRNA expression of p33ING1b and p29ING4 was increased at early and late stages of disease with higher expression of both genes at late stages of disease compared to early stages (Robson stages III/IV vs. I/II) (p33ING1b and p29ING4: stages I/II and III/IV vs. normal tissue p<0.001 and p<0.0001, respectively; p33ING1b and p29ING4: stages III/IV vs. I/II p<0.01 and p<0.001, respectively). (b) Results of the real time RT-PCR were normalized to kidney normal tissue and expressed as x-fold difference (2- ∆∆Ct). Expression of p33ING1b and p29ING4 by renal carcinoma cells was confirmed (Cy3 red; DAPI blue (nuclear counterstaining)). (c) Sections are representative of n=30 patients/group. Representative western blots of p33ING1b and p29ING4 (loading control ß-actin).
Peptide, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 1 article reviews
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94
Rockland Immunochemicals fluorescein conjugated cathelicidin antimicrobial peptide ll 37
Figure 1: Expression of p33ING1b and <t>p29ING4</t> in renal cell carcinoma. (a) mRNA expression of p33ING1b and p29ING4 was increased at early and late stages of disease with higher expression of both genes at late stages of disease compared to early stages (Robson stages III/IV vs. I/II) (p33ING1b and p29ING4: stages I/II and III/IV vs. normal tissue p<0.001 and p<0.0001, respectively; p33ING1b and p29ING4: stages III/IV vs. I/II p<0.01 and p<0.001, respectively). (b) Results of the real time RT-PCR were normalized to kidney normal tissue and expressed as x-fold difference (2- ∆∆Ct). Expression of p33ING1b and p29ING4 by renal carcinoma cells was confirmed (Cy3 red; DAPI blue (nuclear counterstaining)). (c) Sections are representative of n=30 patients/group. Representative western blots of p33ING1b and p29ING4 (loading control ß-actin).
Fluorescein Conjugated Cathelicidin Antimicrobial Peptide Ll 37, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
Novus Biologicals l11s t s
Figure 1: Expression of p33ING1b and <t>p29ING4</t> in renal cell carcinoma. (a) mRNA expression of p33ING1b and p29ING4 was increased at early and late stages of disease with higher expression of both genes at late stages of disease compared to early stages (Robson stages III/IV vs. I/II) (p33ING1b and p29ING4: stages I/II and III/IV vs. normal tissue p<0.001 and p<0.0001, respectively; p33ING1b and p29ING4: stages III/IV vs. I/II p<0.01 and p<0.001, respectively). (b) Results of the real time RT-PCR were normalized to kidney normal tissue and expressed as x-fold difference (2- ∆∆Ct). Expression of p33ING1b and p29ING4 by renal carcinoma cells was confirmed (Cy3 red; DAPI blue (nuclear counterstaining)). (c) Sections are representative of n=30 patients/group. Representative western blots of p33ING1b and p29ING4 (loading control ß-actin).
L11s T S, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Tocris compstatin control peptide
A: The percentage of Mf that had at least one PMN adhered to their surface or indirectly fastened by extracellular DNA at 24 hours post-experimental set up (n = 3). Orange and red bars represent 5% autologous serum and 25% autologous serum treated wells respectively. The autologous serum was either untreated (no peptide control), treated with 100μM inactive <t>compstatin</t> analogue (control peptide) or treated with 100μM active compstatin. Error bars represent standard error of the mean. B: The percentage of Mf that survived 5 days in the presence of both PMNs and PBMCs after treatment of serum with control peptide or compstatin (n = 3). C: PMNs were incubated with blocking antibodies for 2 hours prior to incubation with Mf for 5 days. PMN-mediated killing occurred to the same extent in control (no antibody) wells and those treated with anti-ICAM-1 and anti-Cd11b (p = <0.0001). No significant differences were observed between PMN incubated with Mf with or without the anti-ICAM-1 or anti-Cd11b (n = 3).
Compstatin Control Peptide, supplied by Tocris, 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
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90
Rockland Immunochemicals influenza
A: The percentage of Mf that had at least one PMN adhered to their surface or indirectly fastened by extracellular DNA at 24 hours post-experimental set up (n = 3). Orange and red bars represent 5% autologous serum and 25% autologous serum treated wells respectively. The autologous serum was either untreated (no peptide control), treated with 100μM inactive <t>compstatin</t> analogue (control peptide) or treated with 100μM active compstatin. Error bars represent standard error of the mean. B: The percentage of Mf that survived 5 days in the presence of both PMNs and PBMCs after treatment of serum with control peptide or compstatin (n = 3). C: PMNs were incubated with blocking antibodies for 2 hours prior to incubation with Mf for 5 days. PMN-mediated killing occurred to the same extent in control (no antibody) wells and those treated with anti-ICAM-1 and anti-Cd11b (p = <0.0001). No significant differences were observed between PMN incubated with Mf with or without the anti-ICAM-1 or anti-Cd11b (n = 3).
Influenza, supplied by Rockland Immunochemicals, 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
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85
Rockland Immunochemicals ovalbumin ova
A: The percentage of Mf that had at least one PMN adhered to their surface or indirectly fastened by extracellular DNA at 24 hours post-experimental set up (n = 3). Orange and red bars represent 5% autologous serum and 25% autologous serum treated wells respectively. The autologous serum was either untreated (no peptide control), treated with 100μM inactive <t>compstatin</t> analogue (control peptide) or treated with 100μM active compstatin. Error bars represent standard error of the mean. B: The percentage of Mf that survived 5 days in the presence of both PMNs and PBMCs after treatment of serum with control peptide or compstatin (n = 3). C: PMNs were incubated with blocking antibodies for 2 hours prior to incubation with Mf for 5 days. PMN-mediated killing occurred to the same extent in control (no antibody) wells and those treated with anti-ICAM-1 and anti-Cd11b (p = <0.0001). No significant differences were observed between PMN incubated with Mf with or without the anti-ICAM-1 or anti-Cd11b (n = 3).
Ovalbumin Ova, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 85 stars, based on 1 article reviews
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91
Tocris control peptide
A: The percentage of Mf that had at least one PMN adhered to their surface or indirectly fastened by extracellular DNA at 24 hours post-experimental set up (n = 3). Orange and red bars represent 5% autologous serum and 25% autologous serum treated wells respectively. The autologous serum was either untreated (no peptide control), treated with 100μM inactive <t>compstatin</t> analogue (control peptide) or treated with 100μM active compstatin. Error bars represent standard error of the mean. B: The percentage of Mf that survived 5 days in the presence of both PMNs and PBMCs after treatment of serum with control peptide or compstatin (n = 3). C: PMNs were incubated with blocking antibodies for 2 hours prior to incubation with Mf for 5 days. PMN-mediated killing occurred to the same extent in control (no antibody) wells and those treated with anti-ICAM-1 and anti-Cd11b (p = <0.0001). No significant differences were observed between PMN incubated with Mf with or without the anti-ICAM-1 or anti-Cd11b (n = 3).
Control Peptide, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 91 stars, based on 1 article reviews
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85
Rockland Immunochemicals peptides
A: The percentage of Mf that had at least one PMN adhered to their surface or indirectly fastened by extracellular DNA at 24 hours post-experimental set up (n = 3). Orange and red bars represent 5% autologous serum and 25% autologous serum treated wells respectively. The autologous serum was either untreated (no peptide control), treated with 100μM inactive <t>compstatin</t> analogue (control peptide) or treated with 100μM active compstatin. Error bars represent standard error of the mean. B: The percentage of Mf that survived 5 days in the presence of both PMNs and PBMCs after treatment of serum with control peptide or compstatin (n = 3). C: PMNs were incubated with blocking antibodies for 2 hours prior to incubation with Mf for 5 days. PMN-mediated killing occurred to the same extent in control (no antibody) wells and those treated with anti-ICAM-1 and anti-Cd11b (p = <0.0001). No significant differences were observed between PMN incubated with Mf with or without the anti-ICAM-1 or anti-Cd11b (n = 3).
Peptides, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 85 stars, based on 1 article reviews
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Image Search Results


Figure 1: Expression of p33ING1b and p29ING4 in renal cell carcinoma. (a) mRNA expression of p33ING1b and p29ING4 was increased at early and late stages of disease with higher expression of both genes at late stages of disease compared to early stages (Robson stages III/IV vs. I/II) (p33ING1b and p29ING4: stages I/II and III/IV vs. normal tissue p<0.001 and p<0.0001, respectively; p33ING1b and p29ING4: stages III/IV vs. I/II p<0.01 and p<0.001, respectively). (b) Results of the real time RT-PCR were normalized to kidney normal tissue and expressed as x-fold difference (2- ∆∆Ct). Expression of p33ING1b and p29ING4 by renal carcinoma cells was confirmed (Cy3 red; DAPI blue (nuclear counterstaining)). (c) Sections are representative of n=30 patients/group. Representative western blots of p33ING1b and p29ING4 (loading control ß-actin).

Journal: Journal of Clinical & Cellular Immunology

Article Title: Tumor Suppressor Gene P29ing4 is Overexpressed and Induces a CD8 T Effector Cell Response in Human Renal Cell Carcinoma

doi: 10.4172/2155-9899.1000511

Figure Lengend Snippet: Figure 1: Expression of p33ING1b and p29ING4 in renal cell carcinoma. (a) mRNA expression of p33ING1b and p29ING4 was increased at early and late stages of disease with higher expression of both genes at late stages of disease compared to early stages (Robson stages III/IV vs. I/II) (p33ING1b and p29ING4: stages I/II and III/IV vs. normal tissue p<0.001 and p<0.0001, respectively; p33ING1b and p29ING4: stages III/IV vs. I/II p<0.01 and p<0.001, respectively). (b) Results of the real time RT-PCR were normalized to kidney normal tissue and expressed as x-fold difference (2- ∆∆Ct). Expression of p33ING1b and p29ING4 by renal carcinoma cells was confirmed (Cy3 red; DAPI blue (nuclear counterstaining)). (c) Sections are representative of n=30 patients/group. Representative western blots of p33ING1b and p29ING4 (loading control ß-actin).

Article Snippet: Analysis of single staining was performed for p33ING1 (Santa Cruz Biotechnology, CA, USA), p29ING4 (Rockland/Biomol, Hamburg, Germany) CD4, CD25, Foxp3, CD8, (Abcam, Cambridge, UK), IFN-γ (BD Pharmingen, Heidelberg, Germany), IL-2, and IL-10 (R&D Systems, Minneapolis, USA).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Control

Figure 4: p33ING1b- and p29ING4-specific T cell reactivity. Four peptides resulted in significantly increased expression of IFN-γ compared to controls, independent of tumor stage (p33ING1b (aa109-118) and aa259-268, and p29ING4 (aa149-158) and aa239-248; p<0.001) Stages I/ II (a) and Stages III/IV (b). Elispot analysis was measured as spots/5 x 105 cells/patient.

Journal: Journal of Clinical & Cellular Immunology

Article Title: Tumor Suppressor Gene P29ing4 is Overexpressed and Induces a CD8 T Effector Cell Response in Human Renal Cell Carcinoma

doi: 10.4172/2155-9899.1000511

Figure Lengend Snippet: Figure 4: p33ING1b- and p29ING4-specific T cell reactivity. Four peptides resulted in significantly increased expression of IFN-γ compared to controls, independent of tumor stage (p33ING1b (aa109-118) and aa259-268, and p29ING4 (aa149-158) and aa239-248; p<0.001) Stages I/ II (a) and Stages III/IV (b). Elispot analysis was measured as spots/5 x 105 cells/patient.

Article Snippet: Analysis of single staining was performed for p33ING1 (Santa Cruz Biotechnology, CA, USA), p29ING4 (Rockland/Biomol, Hamburg, Germany) CD4, CD25, Foxp3, CD8, (Abcam, Cambridge, UK), IFN-γ (BD Pharmingen, Heidelberg, Germany), IL-2, and IL-10 (R&D Systems, Minneapolis, USA).

Techniques: Expressing, Enzyme-linked Immunospot

Figure 5: p33ING1b- and p29ING4-specific T cell reactivity. Two peptides resulted in increased expression of IL-10 compared to controls; peptide p33ING1b (aa109-118) at all stages and p29ING4 (aa239-248) at late stages (p<0.001). Stages I/ II (a) and Stages III/IV (b). Luminex analysis was measured as pg/ml.

Journal: Journal of Clinical & Cellular Immunology

Article Title: Tumor Suppressor Gene P29ing4 is Overexpressed and Induces a CD8 T Effector Cell Response in Human Renal Cell Carcinoma

doi: 10.4172/2155-9899.1000511

Figure Lengend Snippet: Figure 5: p33ING1b- and p29ING4-specific T cell reactivity. Two peptides resulted in increased expression of IL-10 compared to controls; peptide p33ING1b (aa109-118) at all stages and p29ING4 (aa239-248) at late stages (p<0.001). Stages I/ II (a) and Stages III/IV (b). Luminex analysis was measured as pg/ml.

Article Snippet: Analysis of single staining was performed for p33ING1 (Santa Cruz Biotechnology, CA, USA), p29ING4 (Rockland/Biomol, Hamburg, Germany) CD4, CD25, Foxp3, CD8, (Abcam, Cambridge, UK), IFN-γ (BD Pharmingen, Heidelberg, Germany), IL-2, and IL-10 (R&D Systems, Minneapolis, USA).

Techniques: Expressing, Luminex

Figure 6: p33ING1b- and p29ING4-specific T cell reactivity. Evaluation of IL-2 expression revealed that only a single epitope (p29ING4 (aa149-158)) resulted in high responsiveness of T cells from RCC patients after stimulation with the peptide (stages I/II vs. III/IV p<0.001). PBMCs from healthy volunteers (n=30) had no significant IL-2 expression after stimulation with all peptide epitopes. Luminex analysis for IL-2 expression was measured as pg/ml and presented as percent stimulation index.

Journal: Journal of Clinical & Cellular Immunology

Article Title: Tumor Suppressor Gene P29ing4 is Overexpressed and Induces a CD8 T Effector Cell Response in Human Renal Cell Carcinoma

doi: 10.4172/2155-9899.1000511

Figure Lengend Snippet: Figure 6: p33ING1b- and p29ING4-specific T cell reactivity. Evaluation of IL-2 expression revealed that only a single epitope (p29ING4 (aa149-158)) resulted in high responsiveness of T cells from RCC patients after stimulation with the peptide (stages I/II vs. III/IV p<0.001). PBMCs from healthy volunteers (n=30) had no significant IL-2 expression after stimulation with all peptide epitopes. Luminex analysis for IL-2 expression was measured as pg/ml and presented as percent stimulation index.

Article Snippet: Analysis of single staining was performed for p33ING1 (Santa Cruz Biotechnology, CA, USA), p29ING4 (Rockland/Biomol, Hamburg, Germany) CD4, CD25, Foxp3, CD8, (Abcam, Cambridge, UK), IFN-γ (BD Pharmingen, Heidelberg, Germany), IL-2, and IL-10 (R&D Systems, Minneapolis, USA).

Techniques: Expressing, Luminex

Figure 7: p29ING4 presentation by MHC class I (a) and II (b) molecules. p29ING4 presentation by major histocompatibility complex (MHC) class I and II antigens was shown to be increased in RCC but not in healthy kidneys.

Journal: Journal of Clinical & Cellular Immunology

Article Title: Tumor Suppressor Gene P29ing4 is Overexpressed and Induces a CD8 T Effector Cell Response in Human Renal Cell Carcinoma

doi: 10.4172/2155-9899.1000511

Figure Lengend Snippet: Figure 7: p29ING4 presentation by MHC class I (a) and II (b) molecules. p29ING4 presentation by major histocompatibility complex (MHC) class I and II antigens was shown to be increased in RCC but not in healthy kidneys.

Article Snippet: Analysis of single staining was performed for p33ING1 (Santa Cruz Biotechnology, CA, USA), p29ING4 (Rockland/Biomol, Hamburg, Germany) CD4, CD25, Foxp3, CD8, (Abcam, Cambridge, UK), IFN-γ (BD Pharmingen, Heidelberg, Germany), IL-2, and IL-10 (R&D Systems, Minneapolis, USA).

Techniques: Immunopeptidomics

A: The percentage of Mf that had at least one PMN adhered to their surface or indirectly fastened by extracellular DNA at 24 hours post-experimental set up (n = 3). Orange and red bars represent 5% autologous serum and 25% autologous serum treated wells respectively. The autologous serum was either untreated (no peptide control), treated with 100μM inactive compstatin analogue (control peptide) or treated with 100μM active compstatin. Error bars represent standard error of the mean. B: The percentage of Mf that survived 5 days in the presence of both PMNs and PBMCs after treatment of serum with control peptide or compstatin (n = 3). C: PMNs were incubated with blocking antibodies for 2 hours prior to incubation with Mf for 5 days. PMN-mediated killing occurred to the same extent in control (no antibody) wells and those treated with anti-ICAM-1 and anti-Cd11b (p = <0.0001). No significant differences were observed between PMN incubated with Mf with or without the anti-ICAM-1 or anti-Cd11b (n = 3).

Journal: PLoS Neglected Tropical Diseases

Article Title: Human Leukocytes Kill Brugia malayi Microfilariae Independently of DNA-Based Extracellular Trap Release

doi: 10.1371/journal.pntd.0005279

Figure Lengend Snippet: A: The percentage of Mf that had at least one PMN adhered to their surface or indirectly fastened by extracellular DNA at 24 hours post-experimental set up (n = 3). Orange and red bars represent 5% autologous serum and 25% autologous serum treated wells respectively. The autologous serum was either untreated (no peptide control), treated with 100μM inactive compstatin analogue (control peptide) or treated with 100μM active compstatin. Error bars represent standard error of the mean. B: The percentage of Mf that survived 5 days in the presence of both PMNs and PBMCs after treatment of serum with control peptide or compstatin (n = 3). C: PMNs were incubated with blocking antibodies for 2 hours prior to incubation with Mf for 5 days. PMN-mediated killing occurred to the same extent in control (no antibody) wells and those treated with anti-ICAM-1 and anti-Cd11b (p = <0.0001). No significant differences were observed between PMN incubated with Mf with or without the anti-ICAM-1 or anti-Cd11b (n = 3).

Article Snippet: For the compstatin inhibition studies, autologous serum was pretreated with either 100μM compstatin (Tocris Bioscience, Avonmouth, Bristol, U.K.) or 100μM compstatin control peptide (Tocris Bioscience, Avonmouth, Bristol, U.K.) for 30 min at 37°C.

Techniques: Control, Incubation, Blocking Assay