Mannose binding lectin defects and autoimmune diseases
0
Citation
18
Reference
10
Related Paper
Abstract:
Complement system has a very important role in our defense against different pathogens and harmful immune complexes.The lectin pathway of complement system is activated by mannose binding lectin leading to complement cascade ending with the removal of these invading pathogens and the injuring immune complexes.Defects in mannose binding lectin were found to be associated with MBL2 gene polymorphisms such as exon 1 polymorphisms and promotor region polymorphisms.These defects were linked to serious autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis.The aim of our review is to provide an overview of mannose binding lectin role in complement system and to outline the information about mannose binding lectin defects with systemic lupus erythematosus and rheumatoid arthritis in addition to the possible related explanations.Mannose binding lectin variants were believed to have an association with these autoimmune disorders by many studies with the presence of conflicted studies as well.Keywords:
C-type lectin
C-type lectin
CD69
Ficolin
MASP1
Cite
Citations (9)
C-type lectin
Galectin
Cite
Citations (2)
Mannose binding lectin (MBL) is an important element of the innate immune system. MBL binding leads to activation and cleavage of C3 and C4 suggesting the role of MBL pathway for opsonization and/ phagocytosis. The role of adaptive immune response in development of pathogenic autoantibodies in various autoimmune diseases is well understood. The link between innate and acquired immunity is helpful for understanding the immunopathogenesis of autoimmune diseases. Evidence that innate immune system could lead to autoimmunity is growing with the major recent concept of autoimmune disease pathogenesis is related to impaired apoptotic cell clearance. MBL have been demonstrated to facilitate clearance of apoptotic cells in vivo and in vitro. Low MBL serum levels resulting in impaired apoptotic clearance have shown to enhance the risk for infection and high MBL serum levels and high MBL activity have been associated with inflammatory autoimmune diseases like Systemic Lupus Erythematosus (SLE) that in turn results in to tissue damage and finally leads to organ damage. Serum MBL levels fluctuate during the course of SLE disease activity and MBL genotypes have been found to be useful in assessing the risk of infection during immunosuppressive treatment the majority of the SLE patients receive. This review focuses on the genetic and molecular characteristics of MBL and discusses MBL disease association in autoimmunity with special emphasis on SLE.
Cite
Citations (22)
C-type lectin
CD69
Lectin pathway
Cite
Citations (0)
Ficolin
Lectin pathway
MASP1
C-type lectin
Collectin
Cite
Citations (9)
Abstract The crystal structures of an L‐type lectin domain from Methanocaldococcus jannaschii in apo and mannose‐bound forms have been determined. A thorough investigation of L‐type lectin domains from several organisms provides insight into the differences in these domains from different kingdoms of life. While the overall fold of the L‐type lectin domain is conserved, differences in the lengths of the carbohydrate‐binding loops and significant variations in the Mn 2+ ‐binding site compared to the Ca 2+ ‐binding site are observed. Furthermore, the sequence and phylogenetic analyses suggest that the archaeal L‐type lectin domain is evolutionarily closer to the plant legume lectins than to its bacterial or animal counterparts. This is the first report of the biochemical, structural, sequence, and phylogenetic analyses of an L‐type lectin domain from archaea and serves to enhance our understanding of the species‐specific differences and evolution of L‐type lectin domains.
C-type lectin
Cite
Citations (2)
CD69
Hapten
Sepharose
Cite
Citations (27)
C-type lectin
CD69
Ficolin
Collectin
Cite
Citations (32)
Pathogenesis
Cite
Citations (8)
Abstract Background Polymorphisms in the mannose‐binding lectin gene reduce serum mannose‐binding lectin levels and are associated with enhanced risk of infection. In a family with recurrent staphylococcal disease presenting as furunculosis or carbuncles, an association with mannose‐binding lectin deficiency was investigated. Materials and methods Levels of functional mannose‐binding lectin were estimated and the genotypes of the mannose‐binding lectin gene were analysed on blood samples, collected from the members of one particular family with a high prevalence of furunculosis. Results Functional mannose‐binding lectin levels in sera of 13 of the 28 members of one family showed deficiency. Furunculosis or carbuncles appeared to be present in nine of the 28 family members, seven of which showing the pBly allele and mannose‐binding lectin deficiency. Four young family members of the second generation were pBly positive and mannose‐binding lectin deficient, but had not shown furunculosis yet. Conclusion Members of a particular family suffering from furunculosis differ from their ‘healthy’ relatives as to mannose‐binding lectin genotypes, indicating the relevance of normal mannose‐binding lectin levels in the defence against staphylococcal disease.
C-type lectin
Cite
Citations (22)