Systemic lupus erythematosus (SLE) is an autoimmune disease in which the complement system plays a role in its pathogenesis. Mannose-binding lectin (MBL) is a serum protein, being a component of innate immune system, it is responsible for lectin pathway of complement activation. The presence of several polymorphisms at the coding regions of the MBL-2 gene, especially single point mutation at codon 54, leads to decreased level and /or functional deficits of MBL, which seems to be a risk factor for occurrence of autoimmune diseases, such as in SLE.