Figure 1
Figure 1. Impaired induction of high-affinity LFA-1 in talin-1 and kindlin-3–deficient neutrophils. (A) Flow cytometric measurement of soluble murine ICAM-1/Fc binding to bone marrow neutrophils isolated from Tln1fl/flMx1-Cre/LysMGFP and Fermt3−/−/LysMGFP mixed chimeric mice. Bone marrow cells exposed to ICAM-1 (20 μg/mL) were stimulated with CXCL1 (10nM, 3 minutes). (B) CXCL1 up-regulates ICAM-1 binding to LFA-1 in wild-type, but not in talin-1 or kindlin-3–deficient neutrophils. Preincubation with a blocking anti–LFA-1 mAb (clone M17/4; 10 μg/mL) was used to determine the dependence of ICAM-1 binding on LFA-1. Data are mean ± SEM fold increase over control (n = 3 each).

Impaired induction of high-affinity LFA-1 in talin-1 and kindlin-3–deficient neutrophils. (A) Flow cytometric measurement of soluble murine ICAM-1/Fc binding to bone marrow neutrophils isolated from Tln1fl/flMx1-Cre/LysMGFP and Fermt3−/−/LysMGFP mixed chimeric mice. Bone marrow cells exposed to ICAM-1 (20 μg/mL) were stimulated with CXCL1 (10nM, 3 minutes). (B) CXCL1 up-regulates ICAM-1 binding to LFA-1 in wild-type, but not in talin-1 or kindlin-3–deficient neutrophils. Preincubation with a blocking anti–LFA-1 mAb (clone M17/4; 10 μg/mL) was used to determine the dependence of ICAM-1 binding on LFA-1. Data are mean ± SEM fold increase over control (n = 3 each).

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