Review



ccr5 antagonist dapta  (Tocris)


Bioz Verified Symbol Tocris is a verified supplier
Bioz Manufacturer Symbol Tocris manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 91
      Buy from Supplier

    Structured Review

    Tocris ccr5 antagonist dapta
    Fig. 1. A) Thermal hyperalgesia evoked by the administration of 100 ng/kg of CCL4 (s.c.; 1 h before testing) and its prevention by the <t>CCR5</t> selective antagonist <t>DAPTA</t> (5 mg/kg, s.c., 1 h before testing). (N = 5–6). **P < 0.01 compared with saline (SAL)-treated group, Tukey's test. On top, a diagram of the experimental design is shown. B) Mice received the i.p. administration of anti-CD3 antibody (1 μg/mouse; N = 5) or the corresponding IgG2bκ isotype (1 μg/mouse; N = 5) and 24 h later, withdrawal latencies were taken before any further treatment (BASAL). Next, mice received the acute administration of CCL4 (100 ng/kg) and 1 h later withdrawal latencies were measured again (n = 5). **P < 0.01 compared with the corresponding basal latencies, Bonferroni's correction. On top, a diagram of the experimental design is shown. C) Effect of i.p. treatment 24 h before with either anti-CD3 antibody (1 μg/mouse; N = 5) or IgG2bκ isotype (1 μg/mouse; N = 5) on the total number of circulating white blood cells, lymphocytes, mid-size cells and granulocytes. Individual data are represented as red (anti-CD3 antibody) or blue (isotype) circles and their mean and corresponding S.E. appears as a short red or blue line, respectively. **P < 0.01 compared with isotype-treated group, Bonferroni's correction. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
    Ccr5 Antagonist Dapta, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ccr5+antagonist+dapta/pm34999112-61-1-6?v=Tocris
    Average 91 stars, based on 26 article reviews
    ccr5 antagonist dapta - by Bioz Stars, 2026-07
    91/100 stars

    Images

    1) Product Images from "Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice."

    Article Title: Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice.

    Journal: Life sciences

    doi: 10.1016/j.lfs.2022.120302

    Fig. 1. A) Thermal hyperalgesia evoked by the administration of 100 ng/kg of CCL4 (s.c.; 1 h before testing) and its prevention by the CCR5 selective antagonist DAPTA (5 mg/kg, s.c., 1 h before testing). (N = 5–6). **P < 0.01 compared with saline (SAL)-treated group, Tukey's test. On top, a diagram of the experimental design is shown. B) Mice received the i.p. administration of anti-CD3 antibody (1 μg/mouse; N = 5) or the corresponding IgG2bκ isotype (1 μg/mouse; N = 5) and 24 h later, withdrawal latencies were taken before any further treatment (BASAL). Next, mice received the acute administration of CCL4 (100 ng/kg) and 1 h later withdrawal latencies were measured again (n = 5). **P < 0.01 compared with the corresponding basal latencies, Bonferroni's correction. On top, a diagram of the experimental design is shown. C) Effect of i.p. treatment 24 h before with either anti-CD3 antibody (1 μg/mouse; N = 5) or IgG2bκ isotype (1 μg/mouse; N = 5) on the total number of circulating white blood cells, lymphocytes, mid-size cells and granulocytes. Individual data are represented as red (anti-CD3 antibody) or blue (isotype) circles and their mean and corresponding S.E. appears as a short red or blue line, respectively. **P < 0.01 compared with isotype-treated group, Bonferroni's correction. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
    Figure Legend Snippet: Fig. 1. A) Thermal hyperalgesia evoked by the administration of 100 ng/kg of CCL4 (s.c.; 1 h before testing) and its prevention by the CCR5 selective antagonist DAPTA (5 mg/kg, s.c., 1 h before testing). (N = 5–6). **P < 0.01 compared with saline (SAL)-treated group, Tukey's test. On top, a diagram of the experimental design is shown. B) Mice received the i.p. administration of anti-CD3 antibody (1 μg/mouse; N = 5) or the corresponding IgG2bκ isotype (1 μg/mouse; N = 5) and 24 h later, withdrawal latencies were taken before any further treatment (BASAL). Next, mice received the acute administration of CCL4 (100 ng/kg) and 1 h later withdrawal latencies were measured again (n = 5). **P < 0.01 compared with the corresponding basal latencies, Bonferroni's correction. On top, a diagram of the experimental design is shown. C) Effect of i.p. treatment 24 h before with either anti-CD3 antibody (1 μg/mouse; N = 5) or IgG2bκ isotype (1 μg/mouse; N = 5) on the total number of circulating white blood cells, lymphocytes, mid-size cells and granulocytes. Individual data are represented as red (anti-CD3 antibody) or blue (isotype) circles and their mean and corresponding S.E. appears as a short red or blue line, respectively. **P < 0.01 compared with isotype-treated group, Bonferroni's correction. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

    Techniques Used: Saline

    Fig. 2. Determination by flow cytometry of CCR5 surface expression on CD3+, CD4+ and CD8+ T-cell subsets coming from peripheral blood collected from naïve mice. Histograms of the left-hand side depict representative examples of the fluorescence distribution (mean fluorescence intensity, MFI) detected in the APC channel (CCR5-APC) in cells coming from one sample showing the fluo rescence for the FMO sample (without CCR5 staining) and its CCR5-stained counterpart obtained in CD3+ (A), CD4+ (B) and CD8+ (C) cells. The graphs of the right-hand side show percentages of cells expressing CCR5 on CD3+ (A), CD4+ (B) and CD8+ (C). Dots correspond to individual values ob tained in each sample and red lines represent the calculated mean and the corresponding S.E. (n = 9). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
    Figure Legend Snippet: Fig. 2. Determination by flow cytometry of CCR5 surface expression on CD3+, CD4+ and CD8+ T-cell subsets coming from peripheral blood collected from naïve mice. Histograms of the left-hand side depict representative examples of the fluorescence distribution (mean fluorescence intensity, MFI) detected in the APC channel (CCR5-APC) in cells coming from one sample showing the fluo rescence for the FMO sample (without CCR5 staining) and its CCR5-stained counterpart obtained in CD3+ (A), CD4+ (B) and CD8+ (C) cells. The graphs of the right-hand side show percentages of cells expressing CCR5 on CD3+ (A), CD4+ (B) and CD8+ (C). Dots correspond to individual values ob tained in each sample and red lines represent the calculated mean and the corresponding S.E. (n = 9). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

    Techniques Used: Flow Cytometry, Expressing, Fluorescence, Staining

    Fig. 9. Graphic explanation of the mechanisms proposed to be involved in the switch from analgesia to hyperalgesia when systemic doses of CCL4 are increased from pg/kg to ng/kg. The administration of 100 ng/kg of CCL4 leads to CCR5 activation and the subsequent release of IL-16 from circulating CD8+ T-cells. The activation by IL-16 of CD4 receptors expressed in CD4+ T-cells could evoke CCR5 desensitization in this lymphocyte subset, thus impeding the release of met-enk responsible on the analgesia evoked by lower doses of CCL4 [3]. Besides, the blood increase of hypernociceptive mediators, such as CCL2, CXCL1 and IL-1α [5] provokes a hyperalgesic response.
    Figure Legend Snippet: Fig. 9. Graphic explanation of the mechanisms proposed to be involved in the switch from analgesia to hyperalgesia when systemic doses of CCL4 are increased from pg/kg to ng/kg. The administration of 100 ng/kg of CCL4 leads to CCR5 activation and the subsequent release of IL-16 from circulating CD8+ T-cells. The activation by IL-16 of CD4 receptors expressed in CD4+ T-cells could evoke CCR5 desensitization in this lymphocyte subset, thus impeding the release of met-enk responsible on the analgesia evoked by lower doses of CCL4 [3]. Besides, the blood increase of hypernociceptive mediators, such as CCL2, CXCL1 and IL-1α [5] provokes a hyperalgesic response.

    Techniques Used: Activation Assay



    Similar Products

    ccr5 antagonist dapta  (Tocris)
    91
    Tocris ccr5 antagonist dapta
    Fig. 1. A) Thermal hyperalgesia evoked by the administration of 100 ng/kg of CCL4 (s.c.; 1 h before testing) and its prevention by the <t>CCR5</t> selective antagonist <t>DAPTA</t> (5 mg/kg, s.c., 1 h before testing). (N = 5–6). **P < 0.01 compared with saline (SAL)-treated group, Tukey's test. On top, a diagram of the experimental design is shown. B) Mice received the i.p. administration of anti-CD3 antibody (1 μg/mouse; N = 5) or the corresponding IgG2bκ isotype (1 μg/mouse; N = 5) and 24 h later, withdrawal latencies were taken before any further treatment (BASAL). Next, mice received the acute administration of CCL4 (100 ng/kg) and 1 h later withdrawal latencies were measured again (n = 5). **P < 0.01 compared with the corresponding basal latencies, Bonferroni's correction. On top, a diagram of the experimental design is shown. C) Effect of i.p. treatment 24 h before with either anti-CD3 antibody (1 μg/mouse; N = 5) or IgG2bκ isotype (1 μg/mouse; N = 5) on the total number of circulating white blood cells, lymphocytes, mid-size cells and granulocytes. Individual data are represented as red (anti-CD3 antibody) or blue (isotype) circles and their mean and corresponding S.E. appears as a short red or blue line, respectively. **P < 0.01 compared with isotype-treated group, Bonferroni's correction. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
    Ccr5 Antagonist Dapta, 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
    https://www.bioz.com/product/ccr5+antagonist+dapta/pm34999112-61-1-6?v=Tocris
    Average 91 stars, based on 1 article reviews
    ccr5 antagonist dapta - by Bioz Stars, 2026-07
    91/100 stars
    		  Buy from Supplier
    ccr5 antagonist d-ala 1 -peptide t-nh 2 ; dapta  (Bachem)
    90
    Bachem ccr5 antagonist d-ala 1 -peptide t-nh 2 ; dapta
    Mean clinical scores of age- and sex-matched control mice after saline and <t>CCR5</t> +/+ and CCR5 −/− mice after induction of EAE with MOG 35-55 A. Control mice group had no symptoms B. Maximal mean score was 1.8±0.2 in MOG 35-55 -immunized CCR5 −/− mice and 3.1±1.2 in MOG 35-55 -immunized CCR5 +/+ mice. Mean day of onset was the same for CCR5 +/+ (11.8±1.8) and CCR5 −/− (11.2±1.8) mice. Mean body weight (g) was compared to day 0 in each group after injection of saline or MOG 35-55 for 28 days C. At day 28, control mouse body weight had increased 3.8±2.2 g, but had decreased 3.2±3.2 g and 2.6±3.0 g in MOG35-55-immunized CCR5 +/+ and CCR5 −/− mice, respectively. Weight loss (%) was not different between MOG 35-55 -induced CCR5 +/+ (14.6±13.8) and CCR5 −/− (11.4±13.4) mice D. Values are presented as mean ± SEM. # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.
    Ccr5 Antagonist D Ala 1 Peptide T Nh 2 ; Dapta, supplied by Bachem, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ccr5+antagonist+dapta/pmc04941248-116-25-34?v=Bachem
    Average 90 stars, based on 1 article reviews
    ccr5 antagonist d-ala 1 -peptide t-nh 2 ; dapta - by Bioz Stars, 2026-07
    90/100 stars
    		  Buy from Supplier
    ccr5 antagonist d ala peptide t amide  (Tocris)
    93
    Tocris ccr5 antagonist d ala peptide t amide
    Mean clinical scores of age- and sex-matched control mice after saline and <t>CCR5</t> +/+ and CCR5 −/− mice after induction of EAE with MOG 35-55 A. Control mice group had no symptoms B. Maximal mean score was 1.8±0.2 in MOG 35-55 -immunized CCR5 −/− mice and 3.1±1.2 in MOG 35-55 -immunized CCR5 +/+ mice. Mean day of onset was the same for CCR5 +/+ (11.8±1.8) and CCR5 −/− (11.2±1.8) mice. Mean body weight (g) was compared to day 0 in each group after injection of saline or MOG 35-55 for 28 days C. At day 28, control mouse body weight had increased 3.8±2.2 g, but had decreased 3.2±3.2 g and 2.6±3.0 g in MOG35-55-immunized CCR5 +/+ and CCR5 −/− mice, respectively. Weight loss (%) was not different between MOG 35-55 -induced CCR5 +/+ (14.6±13.8) and CCR5 −/− (11.4±13.4) mice D. Values are presented as mean ± SEM. # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.
    Ccr5 Antagonist D Ala Peptide T Amide, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ccr5+antagonist+dapta/pmc04136330-105-1-7?v=Tocris
    Average 93 stars, based on 1 article reviews
    ccr5 antagonist d ala peptide t amide - by Bioz Stars, 2026-07
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    Fig. 1. A) Thermal hyperalgesia evoked by the administration of 100 ng/kg of CCL4 (s.c.; 1 h before testing) and its prevention by the CCR5 selective antagonist DAPTA (5 mg/kg, s.c., 1 h before testing). (N = 5–6). **P < 0.01 compared with saline (SAL)-treated group, Tukey's test. On top, a diagram of the experimental design is shown. B) Mice received the i.p. administration of anti-CD3 antibody (1 μg/mouse; N = 5) or the corresponding IgG2bκ isotype (1 μg/mouse; N = 5) and 24 h later, withdrawal latencies were taken before any further treatment (BASAL). Next, mice received the acute administration of CCL4 (100 ng/kg) and 1 h later withdrawal latencies were measured again (n = 5). **P < 0.01 compared with the corresponding basal latencies, Bonferroni's correction. On top, a diagram of the experimental design is shown. C) Effect of i.p. treatment 24 h before with either anti-CD3 antibody (1 μg/mouse; N = 5) or IgG2bκ isotype (1 μg/mouse; N = 5) on the total number of circulating white blood cells, lymphocytes, mid-size cells and granulocytes. Individual data are represented as red (anti-CD3 antibody) or blue (isotype) circles and their mean and corresponding S.E. appears as a short red or blue line, respectively. **P < 0.01 compared with isotype-treated group, Bonferroni's correction. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

    Journal: Life sciences

    Article Title: Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice.

    doi: 10.1016/j.lfs.2022.120302

    Figure Lengend Snippet: Fig. 1. A) Thermal hyperalgesia evoked by the administration of 100 ng/kg of CCL4 (s.c.; 1 h before testing) and its prevention by the CCR5 selective antagonist DAPTA (5 mg/kg, s.c., 1 h before testing). (N = 5–6). **P < 0.01 compared with saline (SAL)-treated group, Tukey's test. On top, a diagram of the experimental design is shown. B) Mice received the i.p. administration of anti-CD3 antibody (1 μg/mouse; N = 5) or the corresponding IgG2bκ isotype (1 μg/mouse; N = 5) and 24 h later, withdrawal latencies were taken before any further treatment (BASAL). Next, mice received the acute administration of CCL4 (100 ng/kg) and 1 h later withdrawal latencies were measured again (n = 5). **P < 0.01 compared with the corresponding basal latencies, Bonferroni's correction. On top, a diagram of the experimental design is shown. C) Effect of i.p. treatment 24 h before with either anti-CD3 antibody (1 μg/mouse; N = 5) or IgG2bκ isotype (1 μg/mouse; N = 5) on the total number of circulating white blood cells, lymphocytes, mid-size cells and granulocytes. Individual data are represented as red (anti-CD3 antibody) or blue (isotype) circles and their mean and corresponding S.E. appears as a short red or blue line, respectively. **P < 0.01 compared with isotype-treated group, Bonferroni's correction. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: The CCR5 antagonist DAPTA (5 mg/kg; Tocris), the opioid receptor antagonist naloxone (3 mg/kg; Tocris) and the selective δ-opioid receptor antagonist naltrindole (1 mg/kg; Tocris) were dissolved in saline and administered s.c. 1 h, 15 min and 30 min before testing, respectively.

    Techniques: Saline

    Fig. 2. Determination by flow cytometry of CCR5 surface expression on CD3+, CD4+ and CD8+ T-cell subsets coming from peripheral blood collected from naïve mice. Histograms of the left-hand side depict representative examples of the fluorescence distribution (mean fluorescence intensity, MFI) detected in the APC channel (CCR5-APC) in cells coming from one sample showing the fluo rescence for the FMO sample (without CCR5 staining) and its CCR5-stained counterpart obtained in CD3+ (A), CD4+ (B) and CD8+ (C) cells. The graphs of the right-hand side show percentages of cells expressing CCR5 on CD3+ (A), CD4+ (B) and CD8+ (C). Dots correspond to individual values ob tained in each sample and red lines represent the calculated mean and the corresponding S.E. (n = 9). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

    Journal: Life sciences

    Article Title: Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice.

    doi: 10.1016/j.lfs.2022.120302

    Figure Lengend Snippet: Fig. 2. Determination by flow cytometry of CCR5 surface expression on CD3+, CD4+ and CD8+ T-cell subsets coming from peripheral blood collected from naïve mice. Histograms of the left-hand side depict representative examples of the fluorescence distribution (mean fluorescence intensity, MFI) detected in the APC channel (CCR5-APC) in cells coming from one sample showing the fluo rescence for the FMO sample (without CCR5 staining) and its CCR5-stained counterpart obtained in CD3+ (A), CD4+ (B) and CD8+ (C) cells. The graphs of the right-hand side show percentages of cells expressing CCR5 on CD3+ (A), CD4+ (B) and CD8+ (C). Dots correspond to individual values ob tained in each sample and red lines represent the calculated mean and the corresponding S.E. (n = 9). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: The CCR5 antagonist DAPTA (5 mg/kg; Tocris), the opioid receptor antagonist naloxone (3 mg/kg; Tocris) and the selective δ-opioid receptor antagonist naltrindole (1 mg/kg; Tocris) were dissolved in saline and administered s.c. 1 h, 15 min and 30 min before testing, respectively.

    Techniques: Flow Cytometry, Expressing, Fluorescence, Staining

    Fig. 9. Graphic explanation of the mechanisms proposed to be involved in the switch from analgesia to hyperalgesia when systemic doses of CCL4 are increased from pg/kg to ng/kg. The administration of 100 ng/kg of CCL4 leads to CCR5 activation and the subsequent release of IL-16 from circulating CD8+ T-cells. The activation by IL-16 of CD4 receptors expressed in CD4+ T-cells could evoke CCR5 desensitization in this lymphocyte subset, thus impeding the release of met-enk responsible on the analgesia evoked by lower doses of CCL4 [3]. Besides, the blood increase of hypernociceptive mediators, such as CCL2, CXCL1 and IL-1α [5] provokes a hyperalgesic response.

    Journal: Life sciences

    Article Title: Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice.

    doi: 10.1016/j.lfs.2022.120302

    Figure Lengend Snippet: Fig. 9. Graphic explanation of the mechanisms proposed to be involved in the switch from analgesia to hyperalgesia when systemic doses of CCL4 are increased from pg/kg to ng/kg. The administration of 100 ng/kg of CCL4 leads to CCR5 activation and the subsequent release of IL-16 from circulating CD8+ T-cells. The activation by IL-16 of CD4 receptors expressed in CD4+ T-cells could evoke CCR5 desensitization in this lymphocyte subset, thus impeding the release of met-enk responsible on the analgesia evoked by lower doses of CCL4 [3]. Besides, the blood increase of hypernociceptive mediators, such as CCL2, CXCL1 and IL-1α [5] provokes a hyperalgesic response.

    Article Snippet: The CCR5 antagonist DAPTA (5 mg/kg; Tocris), the opioid receptor antagonist naloxone (3 mg/kg; Tocris) and the selective δ-opioid receptor antagonist naltrindole (1 mg/kg; Tocris) were dissolved in saline and administered s.c. 1 h, 15 min and 30 min before testing, respectively.

    Techniques: Activation Assay

    Mean clinical scores of age- and sex-matched control mice after saline and CCR5 +/+ and CCR5 −/− mice after induction of EAE with MOG 35-55 A. Control mice group had no symptoms B. Maximal mean score was 1.8±0.2 in MOG 35-55 -immunized CCR5 −/− mice and 3.1±1.2 in MOG 35-55 -immunized CCR5 +/+ mice. Mean day of onset was the same for CCR5 +/+ (11.8±1.8) and CCR5 −/− (11.2±1.8) mice. Mean body weight (g) was compared to day 0 in each group after injection of saline or MOG 35-55 for 28 days C. At day 28, control mouse body weight had increased 3.8±2.2 g, but had decreased 3.2±3.2 g and 2.6±3.0 g in MOG35-55-immunized CCR5 +/+ and CCR5 −/− mice, respectively. Weight loss (%) was not different between MOG 35-55 -induced CCR5 +/+ (14.6±13.8) and CCR5 −/− (11.4±13.4) mice D. Values are presented as mean ± SEM. # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

    Journal: Oncotarget

    Article Title: CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice

    doi: 10.18632/oncotarget.8097

    Figure Lengend Snippet: Mean clinical scores of age- and sex-matched control mice after saline and CCR5 +/+ and CCR5 −/− mice after induction of EAE with MOG 35-55 A. Control mice group had no symptoms B. Maximal mean score was 1.8±0.2 in MOG 35-55 -immunized CCR5 −/− mice and 3.1±1.2 in MOG 35-55 -immunized CCR5 +/+ mice. Mean day of onset was the same for CCR5 +/+ (11.8±1.8) and CCR5 −/− (11.2±1.8) mice. Mean body weight (g) was compared to day 0 in each group after injection of saline or MOG 35-55 for 28 days C. At day 28, control mouse body weight had increased 3.8±2.2 g, but had decreased 3.2±3.2 g and 2.6±3.0 g in MOG35-55-immunized CCR5 +/+ and CCR5 −/− mice, respectively. Weight loss (%) was not different between MOG 35-55 -induced CCR5 +/+ (14.6±13.8) and CCR5 −/− (11.4±13.4) mice D. Values are presented as mean ± SEM. # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

    Article Snippet: Cells were maintained in a humidified incubator at 37°C and 5% CO 2 , and were treated simultaneously with con A (4 μg/mL) and a CCR5 antagonist (D-Ala 1 -peptide T-NH 2 ; DAPTA; Bachem Bioscience Inc., King of Prussia, PA) (10 μM) dissolved in distilled water.

    Techniques: Control, Saline, Injection

    Cell infiltration A. and demyelination B. was greater in MOG 35-55 -immunized CCR5 +/+ mice than in MOG 35-55 -immunized CCR5 −/− mice.

    Journal: Oncotarget

    Article Title: CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice

    doi: 10.18632/oncotarget.8097

    Figure Lengend Snippet: Cell infiltration A. and demyelination B. was greater in MOG 35-55 -immunized CCR5 +/+ mice than in MOG 35-55 -immunized CCR5 −/− mice.

    Article Snippet: Cells were maintained in a humidified incubator at 37°C and 5% CO 2 , and were treated simultaneously with con A (4 μg/mL) and a CCR5 antagonist (D-Ala 1 -peptide T-NH 2 ; DAPTA; Bachem Bioscience Inc., King of Prussia, PA) (10 μM) dissolved in distilled water.

    Techniques:

    TNF-α protein expression in MOG 35-55 -immunized CCR5 +/+ and CCR5 −/− mouse spinal cords B. IFN-γ expression was not significantly different between MOG 35-55 -immunized CCR5 +/+ and CCR5 −/− mouse spinal cords C. MOG 35-55 injection increased IL-1β expression in CCR5 +/+ mice compared to CCR5 −/− mice D. MCP-1 expression in MOG 35-55 -immunized CCR5 +/+ mice was higher than in CCE5 −/− mice. Values are presented as mean ± SEM. * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

    Journal: Oncotarget

    Article Title: CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice

    doi: 10.18632/oncotarget.8097

    Figure Lengend Snippet: TNF-α protein expression in MOG 35-55 -immunized CCR5 +/+ and CCR5 −/− mouse spinal cords B. IFN-γ expression was not significantly different between MOG 35-55 -immunized CCR5 +/+ and CCR5 −/− mouse spinal cords C. MOG 35-55 injection increased IL-1β expression in CCR5 +/+ mice compared to CCR5 −/− mice D. MCP-1 expression in MOG 35-55 -immunized CCR5 +/+ mice was higher than in CCE5 −/− mice. Values are presented as mean ± SEM. * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

    Article Snippet: Cells were maintained in a humidified incubator at 37°C and 5% CO 2 , and were treated simultaneously with con A (4 μg/mL) and a CCR5 antagonist (D-Ala 1 -peptide T-NH 2 ; DAPTA; Bachem Bioscience Inc., King of Prussia, PA) (10 μM) dissolved in distilled water.

    Techniques: Expressing, Injection, Control

    CD3 + , CD4 + , CD8 + T cells did not infiltrate control mouse spinal cord tissue. MOG 35-55 -induced mouse spinal cord tissues showed infiltrating CD3 + , CD4 + , CD8 + T cells A. - C. Values are presented as mean ± SEM. ( n = 3) * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

    Journal: Oncotarget

    Article Title: CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice

    doi: 10.18632/oncotarget.8097

    Figure Lengend Snippet: CD3 + , CD4 + , CD8 + T cells did not infiltrate control mouse spinal cord tissue. MOG 35-55 -induced mouse spinal cord tissues showed infiltrating CD3 + , CD4 + , CD8 + T cells A. - C. Values are presented as mean ± SEM. ( n = 3) * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

    Article Snippet: Cells were maintained in a humidified incubator at 37°C and 5% CO 2 , and were treated simultaneously with con A (4 μg/mL) and a CCR5 antagonist (D-Ala 1 -peptide T-NH 2 ; DAPTA; Bachem Bioscience Inc., King of Prussia, PA) (10 μM) dissolved in distilled water.

    Techniques: Control

    CNPase (myelinating oligodendrocyte marker) A. and NG2 (oligodendrocyte precursor maker) B. expression decreased in MOG 35-55 -induced CCR5 +/+ mouse spinal cords as compared to CCR5 −/− mice spinal cord. Values are presented as mean ± SEM. ( n = 3) * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

    Journal: Oncotarget

    Article Title: CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice

    doi: 10.18632/oncotarget.8097

    Figure Lengend Snippet: CNPase (myelinating oligodendrocyte marker) A. and NG2 (oligodendrocyte precursor maker) B. expression decreased in MOG 35-55 -induced CCR5 +/+ mouse spinal cords as compared to CCR5 −/− mice spinal cord. Values are presented as mean ± SEM. ( n = 3) * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

    Article Snippet: Cells were maintained in a humidified incubator at 37°C and 5% CO 2 , and were treated simultaneously with con A (4 μg/mL) and a CCR5 antagonist (D-Ala 1 -peptide T-NH 2 ; DAPTA; Bachem Bioscience Inc., King of Prussia, PA) (10 μM) dissolved in distilled water.

    Techniques: Marker, Expressing, Control