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NDT Advance Access originally published online on August 3, 2007
Nephrology Dialysis Transplantation 2007 22(12):3370-3377; doi:10.1093/ndt/gfm524
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


Mannose-binding lectin and the kidney

Anja Roos1,2, Mohamed R. Daha2, Johannes van Pelt1 and Stefan P. Berger2

1Department of Clinical Chemistry and 2Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands

Correspondence to: Anja Roos, PhD, Department of Clinical Chemistry, L2-27, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands. Email: A.Roos@LUMC.NL

Keywords: complement; diabetes; ficolin; IgA nephropathy; ischaemia/reperfusion injury; lectin pathway; mannose binding lectin; transplantation

The first 150 words of the full text of this article appear below.



   Introduction
 
The complement system is a key component of innate immunity that plays a major role in host defense against invading pathogens. This is effectuated by a direct attack of pathogens, by mediating inflammation and opsonin-dependent phagocytosis, and by induction and amplification of adaptive immunity. In recent years, it has become increasingly clear that the complement system also plays an important role in immune homeostasis in the healthy situation. In this respect, genetic complement deficiencies are not only associated with infectious diseases, but also with auto-immune and inflammatory diseases. Among the complement deficiencies described in humans, deficiency of the complement factor mannose-binding lectin (MBL) has the highest frequency. Due to its large genetic heterogeneity, MBL is a highly interesting and attractive object of study, and many studies have now revealed the association of a variety of human diseases with the MBL status, being either MBL-deficient or MBL-sufficient. These studies demonstrate that . . . [Full Text of this Article]



   MBL and the lectin pathway of complement
 


   MBL and IgA nephropathy
 


   MBL and diabetic nephropathy
 


   MBL and I/R injury
 


   MBL and renal transplantation
 


   MBL and the kidney: conclusions
 

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