The Role of Mannose-binding Lectin in Systemic Lupus Erythematosus

Overview

Journal Clin Rheumatol

Publisher Springer

Specialty Rheumatology

Date 2008 Jan 25

PMID 18214570

Citations 27

Authors

Odirlei Andre Monticielo

Tamara Mucenic

Ricardo Machado Xavier

Joao Carlos Tavares Brenol

Jose Artur Bogo Chies

Affiliations

Soon will be listed here.

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.

Citing Articles

Late Onset Systemic Lupus Erythematosus - Clinical and Autoantibody Profile and its Comparison with Young Onset Systemic Lupus Erythematosus.

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Interaction between Long Noncoding RNAs and Syncytin-1/Syncytin-2 Genes and Transcripts: How Noncoding RNAs May Affect Pregnancy in Patients with Systemic Lupus Erythematosus.

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Trends in oligomannosylation and α1,2-mannosidase expression in human cancers.

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Association between complement gene polymorphisms and systemic lupus erythematosus: a systematic review and meta-analysis.

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