John Libbey Eurotext



Leukocyte and platelet integrin activation and adhesion Volume 12, issue 1, Janvier-Février 2006


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INSERM U507, Hôpital Necker, 161 rue de Sèvres, 75015 Paris
  • Key words: neutrophil, platelet, integrin, adhesion, LAD
  • Page(s) : 21-33
  • Published in: 2006

A peculiar feature of leukocytes and platelets is their rapid switching from a circulating to an adhesive status, upon activation by inflammation or thrombotic stimuli. This is due to the rapid conformational change of their integrins, which acquire an affinity for adhesion substrates. Complex “inside-out” signaling pathways lead to β 2 integrin activation in leukocytes and α IIbβ 3 integrin activation in platelets. Patients with leukocyte adhesion deficiency type III (LAD-III or LAD1-variant) suffer from recurrent infection and from easy bruising, due to a defective “inside-out” signaling that prevents integrin activation in both leukocytes and platelets. This adhesion deficiency underscores common features of “inside-out” signaling leading to integrins activation in hematopoietic cells. The present review is focused on neutrophil β 2 integrins and platelet α IIbβ 3 integrin. It gives the most recent data on integrins structure and describes the conformational change leading to the high affinity for ligands. Neutrophil and platelet functions involving integrins are detailed. It reviews extensively the present knowledge on integrin “inside-out” signaling pathways triggered by various stimuli in hematopoietic cells.