Liposome mediated drug delivery for leukocyte adhesion deficieny I (LAD I): Targeting the mutated gene ITGB2 and expression of CD18 protein

Abstract

Leukocyte adhesion deficiency (LAD) I is a disorder caused due to mutations in a gene (ITGB2) located on chromosome 21 and encodes the β2 subunit of the leukocyte integrin molecules. This leads to defects in the adhesion of leukocytes on endothelial cells which further leads to recurrent microbial infections due to a decrease in the immune response. Base Excision Repair Mechanism (BER) is instrumental in repairing damaged DNA by removing mutated/damaged bases. We have proposed a hypothesis for the treatment of LAD I by making use of the proteins/enzyme complexes responsible for base excision repair mechanism be introduced into the leukocytes via liposomes. This will target the mutated gene in the leukocytes (mostly neutrophils) and DNA repair will occur. The liposomes can be introduced into the patients via intravenous methods.

Graphical abstract

Keywords

CD18 / β-integrin / LAD I / liposome / BER / ITGB2

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Acknowledgements

The authors thank the management of the VIT University for providing the facilities to carry out this study.

Conflict of interest

Subathra, Kritika, Payal, Tyagi and Mohanasrinivasan declare that they have no conflict of interest.

RIGHTS & PERMISSIONS

2014 Higher Education Press and Springer-Verlag Berlin Heidelberg