normal rat serum nrs  (Jackson Immuno)

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

Article Title: CD8 T cell-initiated blood-brain barrier disruption is independent of neutrophil support.

doi: 10.4049/jimmunol.1200658

Figure Lengend Snippet: FIGURE 2. Efficacy of mAb RB6-8C5 and 1A8 neutrophil-depletion strategies during acute TMEV infection. Histograms showing the efficacy of neutrophil-depletion strategies in representative 7-d TMEV-infected C57BL/6 mice (n = 6/group) using NRS (A, D), RB6-8C5 (B, E), or 1A8 (C, F). Neutrophil-depletion Abs were administered on days 5–7 post-TMEV infection. The CD45hi population was gated and analyzed for the percentages of either GR-1+ or Ly-6G+ cells. (B) RB6-8C5 significantly depleted GR-1+ cells (p , 0.001 by Student t test), and (F) 1A8 significantly depleted Ly-6G+

Article Snippet: Mice were administered 250 mg anti–GR-1 mAb RB6-8C5 (#BE0075; BioXCell), 500 mg anti–Ly-6G mAB 1A8 (#BE0075-1; BioXCell), or 500 mg normal rat serum (NRS) (#89531; Jackson ImmunoResearch Laboratories) on days 5–7 post-TMEV infection.

Techniques: Infection

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

Article Title: CD8 T cell-initiated blood-brain barrier disruption is independent of neutrophil support.

doi: 10.4049/jimmunol.1200658

Figure Lengend Snippet: FIGURE 3. The anti–GR-1 mAb RB6-8C5 depletes CNS-infiltrating CD8+ cells in mice administered VP2121–130 peptide to induce PIFS. Representative contour plots showing the effect of treatment with NRS (A), RB6-8C5 (B), and 1A8 (C) on the percentage of CD45+ cells that are also CD8+. (D) The CD45hi

Article Snippet: Mice were administered 250 mg anti–GR-1 mAb RB6-8C5 (#BE0075; BioXCell), 500 mg anti–Ly-6G mAB 1A8 (#BE0075-1; BioXCell), or 500 mg normal rat serum (NRS) (#89531; Jackson ImmunoResearch Laboratories) on days 5–7 post-TMEV infection.

Techniques:

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

Article Title: CD8 T cell-initiated blood-brain barrier disruption is independent of neutrophil support.

doi: 10.4049/jimmunol.1200658

Figure Lengend Snippet: FIGURE 4. Neutrophil depletion with mAb 1A8 does not preserve BBB tight junctions in CD8 T cell- initiated BBB disruption. (A) Confocal microscopic im- ages from a representative negative control 7-d TMEV- infected C57BL/6 mouse administered mock E7 peptide depict a preservation of vascular integrity and intact tight junction proteins claudin-5 and occludin. Treatment with NRS (B) or depletion of neutrophils with 1A8 mAb treatment (D) is ineffective in reducing degradation of the BBB tight junction proteins claudin-5 and occludin in areas of vascular permeability, as seen through FITC- albumin leakage. Mice treated with RB6-8C5 (C) dis- play a preservation of vascular integrity and intact tight junction proteins on microvessels. All images were acquired at 360 original magnification. Shown are representative images from each of the treatment groups (n = 3/group).

Article Snippet: Mice were administered 250 mg anti–GR-1 mAb RB6-8C5 (#BE0075; BioXCell), 500 mg anti–Ly-6G mAB 1A8 (#BE0075-1; BioXCell), or 500 mg normal rat serum (NRS) (#89531; Jackson ImmunoResearch Laboratories) on days 5–7 post-TMEV infection.

Techniques: Disruption, Negative Control, Infection, Preserving, Permeability

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

Article Title: CD8 T cell-initiated blood-brain barrier disruption is independent of neutrophil support.

doi: 10.4049/jimmunol.1200658

Figure Lengend Snippet: FIGURE 5. Neutrophil depletion with mAb 1A8 does not preserve vas- cular integrity as measured by 3D volumetric analysis of gadolinium en- hancement visible on T1-weighted MRI. Gadolinium-enhanced T1-weighted MRI images showing the extent of vascular permeability in a representative 7-d TMEV-infected mock E7 peptide administered C57BL/6 mouse not undergoing PIFS (A). In (B)–(D), C57BL/6 mice undergoing PIFS were treated with NRS (B), RB6-8C5 (C), or 1A8 (D). (E)–(H) show 3D trans- parency rendering of gadolinium-enhancing areas generated in Analyze 10.0 (Biomedical Imaging Resource, Mayo Clinic) in the same animals. Red areas represent subvolumes with gadolinium enhancement. The intensity of red areas is influenced by the overall thickness of underlying gadolinium- enhancing volume and by distance from surface. (I) Quantification of the 3D volume of vascular permeability in each of the three treatment groups. Treatment with anti–GR-1 mAb RB6-8C5 (n = 5) significantly reduced vascular permeability as seen through decreased volumes of gadolinium enhancement when compared with treatment with NRS (n = 6) (p , 0.05) and treatment with anti–Ly-6G mAb 1A8 (n = 3; p , 0.05). Significance between groups was determined by an ANOVA followed by Dunn’s method of multiple comparison. Error bars indicate SEM.

Article Snippet: Mice were administered 250 mg anti–GR-1 mAb RB6-8C5 (#BE0075; BioXCell), 500 mg anti–Ly-6G mAB 1A8 (#BE0075-1; BioXCell), or 500 mg normal rat serum (NRS) (#89531; Jackson ImmunoResearch Laboratories) on days 5–7 post-TMEV infection.

Techniques: Permeability, Infection, Generated, Imaging, Comparison