Figure 2
Figure 2. Cbl-b deficiency increases LFA-1–dependent BMDM adhesion. (A) Adhesion of BMDMs to mouse endothelial cells is shown in the absence (□) or presence of PMA (50 ng/mL; ■). (B,C) Adhesion of BMDMs to immobilized ICAM-1 (B) or VCAM-1 (C) is shown in the absence (□) or in the presence of mAb to LFA-1 (20 μg/mL; ■) or mAb to VLA-4 (20 μg/mL; ▩). Cell adhesion is represented as percentage of adherent cells. Data are means plus or minus SD (n = 3). Similar results were observed in 3 separate experiments. (D) Analysis of spreading of WT and Cbl-b−/− BMDMs onto ICAM-1 was performed. Data are represented as percentage of spread cells. (E) The numbers of macrophages at 72 hours after intraperitoneal injection of thioglycollate in Cbl-b+/−LFA-1+/−, Cbl-b−/−LFA-1+/−, Cbl-b+/−LFA-1−/−, or Cbl-b−/−LFA-1−/− mice are shown. Data are expressed as absolute numbers of emigrated macrophages into the peritoneum. Data are means plus or minus SD (n = 4-5 mice/group). *P < .05; #P < .01; ns, nonsignificant.

Cbl-b deficiency increases LFA-1–dependent BMDM adhesion. (A) Adhesion of BMDMs to mouse endothelial cells is shown in the absence (□) or presence of PMA (50 ng/mL; ■). (B,C) Adhesion of BMDMs to immobilized ICAM-1 (B) or VCAM-1 (C) is shown in the absence (□) or in the presence of mAb to LFA-1 (20 μg/mL; ■) or mAb to VLA-4 (20 μg/mL; ▩). Cell adhesion is represented as percentage of adherent cells. Data are means plus or minus SD (n = 3). Similar results were observed in 3 separate experiments. (D) Analysis of spreading of WT and Cbl-b−/− BMDMs onto ICAM-1 was performed. Data are represented as percentage of spread cells. (E) The numbers of macrophages at 72 hours after intraperitoneal injection of thioglycollate in Cbl-b+/−LFA-1+/−, Cbl-b−/−LFA-1+/−, Cbl-b+/−LFA-1−/−, or Cbl-b−/−LFA-1−/− mice are shown. Data are expressed as absolute numbers of emigrated macrophages into the peritoneum. Data are means plus or minus SD (n = 4-5 mice/group). *P < .05; #P < .01; ns, nonsignificant.

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