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.

Low producer MBL genotypes are associated with susceptibility to systemic lupus erythematosus in Odisha, India

“…MBL deficiency results in abnormal clearance of apoptotic cells, over expression of autoantigens and generation of autoantibodies [1]. Plasma levels of MBL have been associated with single nucleotide polymorphisms (SNPs) at promoter and coding region of MBL2 gene [4]. MBL2 gene is located at chromosome 10 (10q11.…”

“…MBL2 gene is located at chromosome 10 (10q11. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21] and comprises of four exons. Three functional SNPs in exon 1 at codons 52 (rs5030737; C > T; Arg > Cys), 54 (rs1800450; G > A; Gly > Asp), and 57 (rs1800451; G > A; Gly > Glu), are known as D, B, and C variants, respectively, whereas A is the common non-mutated allele.…”

<i>MBL2</i> Gene Polymorphism and the Association with Neonatal Sepsis in Egyptian Neonates, a Case Control Study

“…Variations of MBL plasma levels are affected by single nucleotide polymorphisms (SNPs) at promoter and coding segment of MBL2 gene [3].…”

Infections and Systemic Lupus Erythematosus

“…In fact, low levels of MBL are associated with poorer outcomes in severe infections, even in otherwise immunocompetent individuals. In synthesis, a proportion of patients with lupus appear to have increased frequency of infections related to allele variants of MBL; such infections are for the most part from encapsulated bacteria, and most likely owing to defective opsonization (Monticielo et al, 2008;Super et al 1989). …”