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Aberrant expression of CD11b and CD11a underlies impaired neutrophil adhesion in glucose-6-phosphate transporter-deficient mice
- Source :
- The Journal of Immunology. 196:50.1-50.1
- Publication Year :
- 2016
- Publisher :
- The American Association of Immunologists, 2016.
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Abstract
- Neutrophils play an essential role in defense against intruding microorganisms. They are produced in great number in the bone marrow and circulate in blood where they are found in a quiescent state. In response to inflammatory stimuli, neutrophils take different steps-rolling, adhesion, and transmigration-to migrate towards inflammation sites. In this study, we investigated the underlying mechanisms of impaired neutrophil adhesion in glycogen storage disease type Ib (GSD-Ib) which is caused by a deficiency of the glucose-6-phosphate transporter (G6PT). GSD-Ib is characterized not only by disrupted glucose homeostasis but also by neutropenia and neutrophil dysfunction. GSD-Ib mice were infused with a recombinant adeno-associated virus (rAAV) vector expressing human G6PT only in liver to increase their survival. Unlike control mice, GSD-Ib-rAAV mice manifested severe neutropenia in both blood and bone marrow and neutrophils of GSD-Ib-rAAV mice were defective in adhesion to tumor necrosis factor-a-treated epithelial cells and intercellular adhesion molecule 1 and fibrinogen. The β2-integrins including CD11a/CD18 and CD11b/CD18 are recognized as vital players in neutrophil recruitment. Consistent with impaired neutrophil adhesion, the expression of CD11a and CD11b were found to be decreased in neutrophils of GSD-Ib-rAAV mice, compared with that of control mice. Particularly neutrophils of GSD-Ib-rAAV mice showed increased proteolytic degradation of CD11b. Given the central role of β2-integrins in neutrophil adhesion, this alternation of CD11a and CD11b molecules and their effect on neutrophil adhesion probably define a molecular mechanism to neutrophil dysfunction manifested in GSD-Ib.
- Subjects :
- Immunology
Immunology and Allergy
Subjects
Details
- ISSN :
- 15506606 and 00221767
- Volume :
- 196
- Database :
- OpenAIRE
- Journal :
- The Journal of Immunology
- Accession number :
- edsair.doi...........f43d10f222c1a7d15111b53523d4ee1b