Kindlin-3 is required for the stabilization of TCR-stimulated LFA-1:ICAM-1 bonds critical for lymphocyte arrest and spreading on dendritic cells.

摘要: Kindlin-3 is a key lymphocyte function–associated antigen-1 (LFA-1) coactivator deleted in leukocyte adhesion deficiency-III (LAD-III). In the present study, we investigated involvement of this adaptor motility and TCR-triggered arrest on ICAM-1 or dendritic cells (DCs). Kindlin-3–null primary T from LAD-III patient migrated normally major lymph node chemokine CCL21 engaged normal TCR signaling. However, activation lymphocytes failed to trigger robust LFA-1–mediated T-cell spreading ICAM-1–expressing DCs that observed lymphocytes. was also essential for cytoskeletal anchorage LFA-1 heterodimer microclustering within ventral focal dots TCR-stimulated spread ICAM-1. Surprisingly, migrating over acquired expression an epitope associated with conformational headpiece domain, β I. This activated highly responsive ICAM-1–driven stop signals locomoting CCL21, but not their counterparts. We suggest selectively contributes final outside-in stabilization bonds generated between chemokine-primed molecules cell-surface