title: The role of mannose-binding lectin in systemic lupus erythematosus.
abstract: Susceptibility to systemic lupus erythematosus (SLE) is associated with genetic, hormonal, immunological, and environmental factors. Many genes have been related with the appearance of SLE, including several loci that code different complement components and their receptors. Some genetic deficiencies of complement molecules are strongly associated with SLE, probably because these deficiencies could cause decreased clearance of apoptotic cell material. As a consequence of the apoptotic material accumulation, high levels of autoantigens can be presented inappropriately to the immune system in an inflammatory context, resulting in an imbalance on the mechanisms of immunological tolerance, immune system activation, and autoantibody production. Recent studies proposed a role to the mannose-binding lectin (MBL) in the SLE physiopathogenesis. This protein activates the complement system, and the presence of several polymorphisms at the promoter and coding regions of the MBL-2 gene determines alterations at the plasma levels of MBL. Some of these polymorphisms have been associated with SLE susceptibility, as well as with clinical and laboratory typical features of this disease, cardiovascular events, and infections. Besides, it has been described that the presence of anti-MBL autoantibodies in sera of SLE patients can influence MBL plasma levels and its functional activity.
authors.affiliation: Division of Rheumatology, Department of Internal Medicine, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil. omonticielo@yahoo.com.br
authors.forename: Odirlei André
authors.initials: OA
authors.lastname: Monticielo
authors.forename: Tamara
authors.initials: T
authors.lastname: Mucenic
authors.forename: Ricardo Machado
authors.initials: RM
authors.lastname: Xavier
authors.forename: João Carlos Tavares
authors.initials: JC
authors.lastname: Brenol
authors.forename: José Artur Bogo
authors.initials: JA
authors.lastname: Chies
mesh_terms: D001323:Autoantibodies / Q000097:blood; D003165:Complement System Proteins; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D037601:Mannose-Binding Lectin / Q000235:genetics / Q000276:immunology / Q000502:physiology*; D011110:Polymorphism, Genetic / Q000235:genetics; D012307:Risk Factors
chemical_list: D001323:Autoantibodies; D037601:Mannose-Binding Lectin; D003165:Complement System Proteins