Objective. To determine whether dysfunctional or deficient rnannose-binding protein (MBP) variants are found with increased frequency in black patients with systemic lupus erythematosus (SLE) compared with controls.
Methods. Allele-specific polymerase chain reaction amplification of 4 different polymorphic sites was performed on samples from 92 black SLE patients and 86 geographically matched black controls.
Results. Two structural polymorphisms of MBP, associated with low serum levels of MBP, were found with significantly increased frequency in the SLE patient population compared with controls. In contrast, a promoter haplotype associated with particularly high serum levels of MBP was negatively associated with SLE.
Conclusion. Deficiencies of MBP predispose individuals to SLE.
Mannose-binding protein (MBP), a member of the complement system, is a serum protein that plays an important role in host defense. It is a member of the collectin family (1) and is capable of opsonizing bacteria directly (2), activating the classical complement pathway (3), activating the alternative complement pathway (4), and activating macrophages via the C l q receptor (5). Its carbohydrate-recognition domain binds terminal fucose, glucose, mannose, or GlcNAc, but not galactose or sialic acid residues (6). MBP, therefore, distinguishes oligo-