role of mannose binding protein in rheumatoid arthritis
Last reviewed 01/2018
The glycosylation of IgG in patients with rheumatoid arthritis is different from a control population: loss of terminal galactose and N-acetyl glucosamine residues results in exposure of mannose residues.
It is proposed that exposure of MBP to these altered immunoglobulins results in complement activation and inflammation.
Notes:
- complement system is a key component of the innate immunity. The lectin
pathway is one of the three pathways of the complement system and can be triggered
by pattern-recognition receptors, mainly mannose-biding lectin (MBL), ficolins
and collectin 11
- suggested that MBL deficiency is associated with joint erosions and early disease onset of adult rheumatoid arthritis (RA) (2)
Reference:
- Malhotra, R. et al.. Glycosylation changes of IgG associated with rheumatoid arthritis can activate complement via the mannose-binding protein. Nature Medicine 1995; 1: 237-243.
- Garred P et al. Two edged role of mannose binding lectin in rheumatoid arthritis: a cross sectional study. J Rheumatol. 2000 Jan; 27(1):26-34.