Mannose-binding lectin (MBL) and vascular complications in diabetes

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.