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Publication : Crucial functions of the Rap1 effector molecule RAPL in lymphocyte and dendritic cell trafficking.

First Author  Katagiri K Year  2004
Journal  Nat Immunol Volume  5
Issue  10 Pages  1045-51
PubMed ID  15361866 Mgi Jnum  J:92670
Mgi Id  MGI:3054284 Doi  10.1038/ni1111
Citation  Katagiri K, et al. (2004) Crucial functions of the Rap1 effector molecule RAPL in lymphocyte and dendritic cell trafficking. Nat Immunol 5(10):1045-51
abstractText  Immunosurveillance requires the coordinated regulation of chemokines and adhesion molecules to guide immune cell migration. However, the critical molecule for governing the high trafficking capability of immune cells is not clear. Here we show that the effector molecule RAPL is indispensable in the integrin-mediated adhesion and migration of lymphocytes and dendritic cells. RAPL deficiency caused defective chemokine-triggered lymphocyte adhesion and migration to secondary lymphoid organs, resulting in atrophic lymphoid follicles and deficient marginal zone B cells, concomitant with increased immature B cells in the blood. Furthermore, splenic dendritic cells were diminished and defective in adhesion. After being activated with inflammatory stimuli, skin and splenic dendritic cells failed to migrate into either the draining lymph nodes or the white pulp of the spleen. Thus, RAPL is a crucial immune cell trafficking regulator essential for immunosurveillance.
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