Activated LFA-1, not Mac-1, determines the fibronectin adhesion of HSV-1-infected DCs. (A) Flow cytometric analyses of activated CD11b were performed in mock-infected (white columns), HSV-1–UV-infected (gray columns), and HSV-1–infected (black columns) DCs at the indicated time points after infection. Although Mac-1 is only marginally activated at early time points after infection, its activation increases at later time points. (B) Four hours after infection, fibronectin adhesion assays were performed using 20 μg/mL of the β2 activatory antibody KIM185, the LFA-1 blocking antibody NKI-L15, or the Mac-1 blocking antibody Bear-1, respectively. Activation of β2-integrins on mock-infected DCs renders them highly adhesive, although it has no effect on HSV-1–infected DCs. Blocking of Mac-1 on infected cells has no significant effect on DC adhesion to fibronectin, whereas it is strongly reduced by the inhibition of LFA-1. Error bars represent ± SD. ***P < .001. **P < .01. *P < .05. ns indicates not significant. The experiments were repeated at least 3 times independently, and each single adhesion experiment was performed in quadruplicate.