Clinical Rheumatology

, Volume 27, Issue 4, pp 413–419

The role of mannose-binding lectin in systemic lupus erythematosus

  • Odirlei André Monticielo
  • Tamara Mucenic
  • Ricardo Machado Xavier
  • João Carlos Tavares Brenol
  • José Artur Bogo Chies
Review Article

DOI: 10.1007/s10067-008-0838-8

Cite this article as:
Monticielo, O.A., Mucenic, T., Xavier, R.M. et al. Clin Rheumatol (2008) 27: 413. doi:10.1007/s10067-008-0838-8

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.

Keywords

ComplementGeneticsImmunologyMannose-binding lectinRisk factorsSystemic lupus erythematosus

Copyright information

© Clinical Rheumatology 2008

Authors and Affiliations

  • Odirlei André Monticielo
    • 1
    • 3
  • Tamara Mucenic
    • 1
  • Ricardo Machado Xavier
    • 1
  • João Carlos Tavares Brenol
    • 1
  • José Artur Bogo Chies
    • 2
  1. 1.Division of Rheumatology, Department of Internal MedicineHospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do SulPorto AlegreBrazil
  2. 2.Department of GeneticsUniversidade Federal do Rio Grande do SulPorto AlegreBrazil
  3. 3.Serviço de Reumatologia do Hospital de Clínicas de Porto Alegre—HCPAPorto AlegreBrazil