Mice lacking the signaling molecule CalDAG-GEFI represent a model for leukocyte adhesion deficiency type III
J. Clin. Invest. Wolfgang Bergmeier, et al. 117:1699 doi:10.1172/JCI30575 [Go to this article.]

Figure 4
Impaired firm adhesion of leukocytes to mesenteric venules in CalDAG-GEFI^–/– mice. (A) Leukocyte rolling in vivo. The number of rolling leukocytes in WT or CalDAG-GEFI^–/– mice was determined by intravital microscopy. Mice were infused with rhodamine 6G to label circulating leukocytes. Leukocyte rolling was quantified 1–5 minutes after superfusion with 300 nM LTB₄. (B) Firm adhesion. WT or CalDAG-GEFI–deficient leukocytes were considered firmly adherent when they remained stationary for more than 30 seconds. n = 6. (C) Blocking antibodies to β₂ integrin markedly reduce leukocyte adhesion to mesenteric venules. Leukocyte adhesion within the first 5 minutes after LTB₄ superfusion was studied in WT mice infused with PBS or 40 μg anti-β₂ antibodies (β₂ Ab). n = 3. *P < 0.05, ***P < 0.001. No significant difference in leukocyte adhesion was observed between untreated and control IgG–treated WT mice (not shown).