Abstract
The complement system plays a crucial role in the pathogenesis of various inflammatory processes. The lectin pathway of the complement is activated through the recognition of pathogens or altered self-structures by the pattern recognition molecules (PRMs) mannan-binding lectin (MBL), H-ficolin, L-ficolin and M-ficolin in collaboration with MBL-associated serine proteases (MASPs). PRMs reportedly play a role in rheumatoid arthritis (RA), and a recent study indicated a correlation between the concentration of these proteins and RA disease activity. Knowledge regarding the role of lectin pathway proteins in juvenile idiopathic arthritis (JIA) is lacking.
Highlights
The complement system plays a crucial role in the pathogenesis of various inflammatory processes
The lectin pathway of the complement is activated through the recognition of pathogens or altered self-structures by the pattern recognition molecules (PRMs) mannan-binding lectin (MBL), H-ficolin, L-ficolin and M-ficolin in collaboration with MBL-associated serine proteases (MASPs)
PRMs reportedly play a role in rheumatoid arthritis (RA), and a recent study indicated a correlation between the concentration of these proteins and RA disease activity
Summary
The complement system plays a crucial role in the pathogenesis of various inflammatory processes. The lectin pathway of the complement is activated through the recognition of pathogens or altered self-structures by the pattern recognition molecules (PRMs) mannan-binding lectin (MBL), H-ficolin, L-ficolin and M-ficolin in collaboration with MBL-associated serine proteases (MASPs). PRMs reportedly play a role in rheumatoid arthritis (RA), and a recent study indicated a correlation between the concentration of these proteins and RA disease activity. Knowledge regarding the role of lectin pathway proteins in juvenile idiopathic arthritis (JIA) is lacking
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