title: The role of kindlin in neutrophil recruitment to inflammatory sites.
abstract: Since the discovery of the lack of kindlin-3 expression as the reason for the immunopathology leukocyte adhesion deficiency III syndrome, the role of kindlin-3 in inflammatory processes was investigated in a numerous studies. This review gives an overview about recent findings regarding the role of kindlin-3 in neutrophil activation and recruitment.
  
  
  
  Kindlin-3, together with talin-1, contributes essentially to the activation of β2-integrins in neutrophils. During inside-out signaling, kindlin-3 binds to the β-cytoplasmic integrin tail and is indispensable for the integrin conformational shift into the high-affinity ligand binding conformation, but not for the intermediate (extended) conformation. During outside-in signaling (as a consequence of integrin ligand binding) kindlin-3 interacts with distinct signaling molecules and is required for cell-autonomous functions like migration and spreading.
  
  
  
  Leukocyte adhesion deficiency III syndrome, which is caused by absence of kindlin-3, is a rarely occurring disease. However, the investigation of the clinical symptoms as well as the underlying molecular mechanisms gave rise to a huge amount of new insights into the processes of integrin activation in neutrophils and the consequences of defects in these processes.
authors.affiliation: Department of Anaesthesiology, Intensive Care and Pain Medicine, University of Münster, Münster, Germany.
authors.forename: Anika
authors.initials: A
authors.lastname: Stadtmann
authors.forename: Alexander
authors.initials: A
authors.lastname: Zarbock
mesh_terms: D000818:Animals; D002352:Carrier Proteins; D015815:Cell Adhesion Molecules / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D002634:Chemotaxis, Leukocyte / Q000235:genetics / Q000276:immunology; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D016023:Integrins / Q000235:genetics / Q000378:metabolism; D018370:Leukocyte-Adhesion Deficiency Syndrome / Q000209:etiology / Q000378:metabolism; D007962:Leukocytes / Q000502:physiology; D020556:Neutrophil Infiltration; D009504:Neutrophils / Q000502:physiology*; D011485:Protein Binding; D015398:Signal Transduction
chemical_list: D002352:Carrier Proteins; D015815:Cell Adhesion Molecules; D016023:Integrins