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Journal of Biomedicine and Biotechnology
Volume 2012 (2012), Article ID 363246, 8 pages
http://dx.doi.org/10.1155/2012/363246
Review Article

Factors of the Lectin Pathway of Complement Activation and Their Clinical Associations in Neonates

1Laboratory of Immunobiology of Infections, Institute of Medical Biology, Polish Academy of Sciences, Lodowa 106, 93-232 Lodz, Poland
2National Science Laboratory, Scottish National Blood Transfusion Service, Ellen's Glen Road, Edinburgh EH17 7QT, Scotland, UK

Received 15 September 2011; Revised 12 December 2011; Accepted 30 December 2011

Academic Editor: Misao Matsushita

Copyright © 2012 Maciej Cedzynski et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

This paper summarizes the data concerning soluble defense lectins (mannan-binding lectin, M-ficolin, L-ficolin, and H-ficolin) with the unique ability to activate complement and their associated serine proteases (MASPs) in neonates. The clinical importance of deficiencies of these immune factors is presented in aspects of perinatal mortality, premature births, and low birthweight. Prenatal serum concentrations of L-ficolin, H-ficolin, and MASP-2 (and probably M-ficolin) correlate with gestational age and birthweight. The relationship of serum MBL to gestational age is controversial. The MBL2 genotypes XA/O and O/O (associated with low-serum MBL) are associated with perinatal infections, whereas the high serum MBL-conferring A/A genotypes may be associated with prematurity. Low-serum L-ficolin concentrations, but not low-serum H-ficolin concentrations, are also associated with perinatal infections. Much of the literature is inconsistent, and the relationships reported so far require independent confirmation at both gene and protein levels. Our preliminary conclusion is that these soluble defense lectins play a protective role in the neonate, and that insufficiency of such factors contributes to the adverse consequences of prematurity and low birthweight.