Dissemin is shutting down on January 1st, 2025

Published in

American Diabetes Association, Diabetes, 10(54), p. 3002-3006, 2005

DOI: 10.2337/diabetes.54.10.3002

Links

Tools

Export citation

Search in Google Scholar

Elevated Levels of Mannose-Binding Lectin at Clinical Manifestation of Type 1 Diabetes in Juveniles

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

Full text: Download

Green circle
Preprint: archiving allowed
Green circle
Postprint: archiving allowed
Red circle
Published version: archiving forbidden
Data provided by SHERPA/RoMEO

Abstract

Mannose-binding lectin (MBL) is a recognition molecule of the lectin pathway of complement and a key component of innate immunity. MBL polymorphisms have been described that are associated with MBL serum concentration, impaired function, and diabetic complications. We investigated 86 new-onset juvenile type 1 diabetic patients and compared these with their nondiabetic siblings and healthy unrelated control subjects. Polymorphisms of MBL exon 1 and promoter were determined, and serum concentration and MBL-complex activity were measured. Although the genetic polymorphisms of MBL were not different between patients and control subjects, MBL serum concentration as well as MBL complex activity was significantly higher in new-onset diabetic patients compared with their siblings matched for high-producing MBL genotypes (P = 0.0018 and P = 0.0005, respectively). The increase in MBL complex activity in high-MBL–producing patients could only partially be explained by high MBL production, as demonstrated by an increased MBL complex activity–to–MBL concentration ratio (P = 0.004). We conclude that MBL serum concentration and complex activity are increased in early- onset diabetic patients upon manifestation independently of genetic predisposition to high MBL production, indicating a possible role in the immunopathogenesis of type 1 diabetes, in addition to the adaptive islet autoimmunity.