scholarly journals Role of bacteria in leukocyte adhesion deficiency-associated periodontitis

2016 ◽  
Vol 94 ◽  
pp. 21-26 ◽  
Author(s):  
George Hajishengallis ◽  
Niki M. Moutsopoulos
Keyword(s):  
Leukocyte Adhesion ◽  
Leukocyte Adhesion Deficiency

The Role of Fucosylation in Leukocyte Adhesion Deficiency II

2004 ◽  
pp. 53-74
Author(s):  
D. Vestweber ◽  
K. Lühn ◽  
T. Marquardt ◽  
M. Wild
Keyword(s):  
Leukocyte Adhesion ◽  
Leukocyte Adhesion Deficiency

scholarly journals Skap2 is required for β2 integrin–mediated neutrophil recruitment and functions

2017 ◽  
Vol 214 (3) ◽  
pp. 851-874 ◽  
Author(s):  
Mark Boras ◽  
Stephanie Volmering ◽  
Arne Bokemeyer ◽  
Jan Rossaint ◽  
Helena Block ◽  
...  
Keyword(s):  
Actin Polymerization ◽  
Leukocyte Adhesion ◽  
Direct Interaction ◽  
Neutrophil Recruitment ◽  
Integrin Activation ◽  
Leukocyte Adhesion Deficiency ◽  
Β2 Integrin ◽  
Syndrome Protein

Integrin activation is required for neutrophil functions. Impaired integrin activation on neutrophils is the hallmark of leukocyte adhesion deficiency (LAD) syndrome in humans, characterized by impaired leukocyte recruitment and recurrent infections. The Src kinase–associated phosphoprotein 2 (Skap2) is involved in integrin functions in different leukocyte subtypes. However, the role of Skap2 in β2 integrin activation and neutrophil recruitment is unknown. In this study, we demonstrate the crucial role of Skap2 in regulating actin polymerization and binding of talin-1 and kindlin-3 to the β2 integrin cytoplasmic domain, thereby being indispensable for β2 integrin activation and neutrophil recruitment. The direct interaction of Skap2 with the Wiskott–Aldrich syndrome protein via its SH3 domain is critical for integrin activation and neutrophil recruitment in vivo. Furthermore, Skap2 regulates integrin-mediated outside-in signaling events and neutrophil functions. Thus, Skap2 is essential to activate the β2 integrins, and loss of Skap2 function is sufficient to cause a LAD-like phenotype in mice.

Mice Lacking the Signaling Molecule, CalDAG-GEFI, Represent a Mouse Model for Leukocyte Adhesion Deficiency Type III.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 674-674
Author(s):  
Wolfgang Bergmeier ◽  
Tobias Goerge ◽  
Hong-Wei Wang ◽  
Stephen M. Cifuni ◽  
Jill R. Crittenden ◽  
...  
Keyword(s):  
Intracellular Signaling ◽  
Leukocyte Adhesion ◽  
Thrombus Formation ◽  
Neutrophil Infiltration ◽  
Neutrophil Function ◽  
Calcium Flux ◽  
Leukocyte Adhesion Deficiency ◽  
Normal Surface

Abstract Defective inside-out activation of β 1, β 2, and β 3 integrins in platelets and leukocytes is a main characteristic of patients with leukocyte adhesion deficiency (LAD)-III syndrome. We have recently shown that CalDAG-GEFI, a member of the CalDAG-GEF/RasGRP family of intracellular signaling molecules that catalyzes the exchange of GTP for GDP bound to Rap1, plays a key role for the activation of α IIbβ 3 in murine platelets. Here we studied the role of CalDAG-GEFI for neutrophil function as well as the activation of β 1 integrins in platelets. Neutrophils from CalDAG-GEFI−/ − mice showed normal surface expression of key adhesion receptors such as L-selectin, PSGL-1, or β 1/β 2 integrins. Calcium flux, degranulation, and oxygen radical formation were similar in wild-type (WT) and mutant cells. In contrast, β 2 integrin-mediated adhesion to fibrinogen was significantly reduced in cells lacking CalDAG-GEFI when compared to controls. In vivo, CalDAG-GEFI-deficient neutrophils showed normal rolling along stimulated venules, while firm adhesion was almost completely inhibited. A similar defect in firm adhesion was observed in WT mice pre-treated with blocking antibodies against β 2 integrins. To determine the role of CalDAG-GEFI in neutrophil emigration, inflammation was induced in the peritoneum or the skin. In both models, neutrophil infiltration was significantly reduced in CalDAG-GEFI−/ − mice when compared to controls. We further demonstrate that CalDAG-GEFI regulates the activation of β 1 integrins in platelets and that CalDAG-GEFI-deficiency leads to a complete inhibition of arterial thrombus formation in mice. Due to its central role in the activation of β 1, β 2, and β 3 integrins, we propose CalDAG-GEFI as a candidate gene defective in LAD-III patients.

Leukocyte Adhesion Deficiency as a Model for the Study of the Functional Role of LFA-1

1990 ◽  
pp. 95-100 ◽  
Author(s):  
A. Fischer ◽  
B. Lisowska-Grospierre ◽  
F. Mazerolles ◽  
F. Le Deist ◽  
N. Perez ◽  
...  
Keyword(s):  
Functional Role ◽  
Leukocyte Adhesion ◽  
Leukocyte Adhesion Deficiency

scholarly journals Clinical and laboratory findings in patients with leukocyte adhesion deficiency type I: A multicenter study in turkey

2021 ◽  
Author(s):  
Ismail Yaz ◽  
Begum Ozbek ◽  
Hacer Neslihan Bildik ◽  
Cagman Tan ◽  
Sevil Oskay Halacli ◽  
...  
Keyword(s):  
Multicenter Study ◽  
Leukocyte Adhesion ◽  
Type I ◽  
Leukocyte Adhesion Deficiency ◽  
Laboratory Findings ◽  
Deficiency Type

scholarly journals Cytokine Profile of a Holstein Calf with Bovine Leukocyte Adhesion Deficiency during the Acute-Phase Inflammatory Response

2002 ◽  
Vol 64 (12) ◽  
pp. 1141-1143 ◽  
Author(s):  
Hajime NAGAHATA ◽  
Katsuro HAGIWARA ◽  
Masahiko KASAMATSU ◽  
Hidetoshi HIGUCHI ◽  
Takashi KUROSAWA
Keyword(s):  
Inflammatory Response ◽  
Acute Phase ◽  
Leukocyte Adhesion ◽  
Cytokine Profile ◽  
Leukocyte Adhesion Deficiency
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