Figure 7
Figure 7. Neutrophil adhesion in synovial microvessels is reduced in G-CSF−/− mice during CIA and leukocyte trafficking during CIA is Mac-1 dependent. (A) Rolling flux (cells/min) and (B) adhesion (number of adherent cells/100 μm) within the synovial microvessels of WT and G-CSF−/− mice with CIA. *P < .05. Representative multiphoton microscopy images of adherent Gr-1+ cells (red/orange) in synovial microvessels in the knee joint synovium of (C) WT and (D) G-CSF−/− mice when clinical evidence of CIA was apparent in WT mice (days 33-35). (E) Clinical scores (mean ± SEM) in mice treated with either isotype control mAb or Mac-1 blocking mAb (5C6) after the onset of CIA. n = 8 mice per treatment group. The effect of 5C6 on the progression of CIA was compared with an isotype control mAb-treated group of mice within the 1 experiment, as shown here and in Figure 2E. P < .01 during days 1 to 14 of arthritis.

Neutrophil adhesion in synovial microvessels is reduced in G-CSF−/− mice during CIA and leukocyte trafficking during CIA is Mac-1 dependent. (A) Rolling flux (cells/min) and (B) adhesion (number of adherent cells/100 μm) within the synovial microvessels of WT and G-CSF−/− mice with CIA. *P < .05. Representative multiphoton microscopy images of adherent Gr-1+ cells (red/orange) in synovial microvessels in the knee joint synovium of (C) WT and (D) G-CSF−/− mice when clinical evidence of CIA was apparent in WT mice (days 33-35). (E) Clinical scores (mean ± SEM) in mice treated with either isotype control mAb or Mac-1 blocking mAb (5C6) after the onset of CIA. n = 8 mice per treatment group. The effect of 5C6 on the progression of CIA was compared with an isotype control mAb-treated group of mice within the 1 experiment, as shown here and in Figure 2E. P < .01 during days 1 to 14 of arthritis.

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