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Letters to the Editor |
1 Department of Clinical Chemistry/564, and
2 Department of Internal Medicine/541, University Medical Centre Nijmegen, PO Box 9101, 6500 HB Nijmegen, The Netherlands
aAuthor for correspondence. E-mail D.Swinkels@AKC.umcn.nl.
| The first 20% of the full text of this article appears below. |
To the Editor:
Mannose-binding lectin (MBL), a pattern-recognition molecule produced by the liver and present in serum, is an important player in the innate immune system. MBL acts by binding various carbohydrate structures on microbial surfaces, after which it activates the complement system via the lectin pathway. In addition, MBL can promote direct opsonophagocytosis of microorganisms and modulate diverse inflammatory mediators (1).
Deficiency of MBL was first identified in association with a common defect of opsonization in children. Additional studies have identified MBL deficiency as a risk factor for diverse infectious diseases (1). In addition, MBL deficiency has been found to be associated with certain autoimmune diseases (1) and, recently, atherosclerosis (2). MBL deficiency is caused by mutations in the coding and promoter regions of the MBL gene, which have a profound effect on plasma concentrations of the MBL protein.
Three point mutations
The following articles in journals at HighWire Press have cited this article:
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W. W. J. van de Sande, A. Fahal, H. Verbrugh, and A. van Belkum Polymorphisms in Genes Involved in Innate Immunity Predispose Toward Mycetoma Susceptibility J. Immunol., September 1, 2007; 179(5): 3065 - 3074. [Abstract] [Full Text] [PDF] |
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