Abstract
The complement system has evolved over time as an effective part of the immune system,
acting effectively in frontline combat against invading microorganisms. Unfortunately,
any war might involve ”collateral damage”, and emerging data indicate that activation
of the complement system may cause damage to innocent bystander cells and tissues
in some situations. This may apply to complement activation and inflammation as it
occurs following myocardial ischemia and reperfusion, which is know to aggravate the
subsequent myocardial injury; and it has recently been proposed that complement activation
may be an important factor in the development of diabetic renal complications. Mannose-binding
lectin (MBL, also known as mannan-binding lectin) is a plasma protein that activates
the complement cascade after binding to carbohydrate structures. Circulating MBL levels
vary widely from person to person, which is mainly due to frequently occurring polymorphisms
within the encoding gene on chromosome 10. One may speculate that these genetically
determined differences in MBL levels and hence in complement activation may play a
role in existing familial clustering in both cardiovascular disease and diabetes-related
vascular complications. The present review will focus on the function of MBL and the
complement system, and on recent data indicating an association between MBL status
and diabetic micro- and macrovascular complications.
Key words
MBL - Mannose-binding lectin - Diabetic nephropathy - Type 1 diabetes - Complement
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T. K. Hansen, M.D. PhD
Immunoendocrine Research Unit, Medical Department M
Aarhus University Hospital · 8000 Aarhus C · Denmark
Phone: +45 8949 2057
Fax: +45 8949 2010
Email: tkh@dadlnet.dk