Terminal complement pathway activation and low lysis inhibitors in rheumatoid arthritis synovial fluid.
OBJECTIVE
To investigate terminal complement activation and lysis inhibitors in rheumatoid arthritis (RA).


METHODS
C5a, vitronectin and clusterin were quantitated by enzyme immunoassays in plasma and synovial fluid (SF) in RA (n = 30) and osteoarthritis (OA) (n = 11).


RESULTS
In RA the concentration of C5a was 3-fold increased in plasma (21.9 vs 7.2 micrograms/l) and 5-fold increased in SF (7.8 vs 1.7 micrograms/l) compared to OA. The SF/plasma ratios for C5a, vitronectin and clusterin were 0.35, 0.36 and 0.23, respectively, not significantly different in the 2 diseases.


CONCLUSIONS
SF terminal pathway activation in RA combined with low local levels of lysis inhibitors might allow lytic or sublytic attacks on local cells, resulting in inflammation and cell damage.
Høgåsen
K
K
Institute of Immunology and Rheumatology, National Hospital, University of Oslo, Norway.
Mollnes
T E
TE
Harboe
M
M
Götze
O
O
Hammer
H B
HB
Oppermann
M
M
D001172:Arthritis, Rheumatoid / Q000097:blood / Q000276:immunology*; D051152:Clusterin; D003167:Complement Activation; D003179:Complement C3b / Q000032:analysis; D015936:Complement C5a / Q000032:analysis*; D003169:Complement Inactivator Proteins / Q000276:immunology; D006023:Glycoproteins / Q000097:blood*; D006801:Humans; D018832:Molecular Chaperones; D010003:Osteoarthritis / Q000097:blood / Q000276:immunology*; D013582:Synovial Fluid / Q000737:chemistry* / Q000276:immunology; D019096:Vitronectin
C495242:CLU protein, human; D051152:Clusterin; D003169:Complement Inactivator Proteins; D006023:Glycoproteins; D018832:Molecular Chaperones; D019096:Vitronectin; D003179:Complement C3b; D015936:Complement C5a