Perturbation of protease inhibitors and substrates in inflammatory arthritis.
Defective systemic fibrinolysis and articular persistence of fibrinlike material are well recognized in RA. Perturbation of the major plasma protease inhibitors, A1AT, A2MG, and AT III, was explored in RA, psoriatic arthritis, and Reiter's syndrome. Experimental evidence is presented and assessed with respect to the potential role of serine esterases and their inhibitors in the pathophysiology of inflammatory arthritis.
B M
BM
Rothschild
L D
LD
Thompson
D D
DD
Pifer
C M
CM
Chesney
D000328:Adult; D000990:Antithrombin III / Q000097:blood; D001172:Arthritis, Rheumatoid / Q000097:blood*; D001798:Blood Proteins; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000032:analysis; D010958:Plasminogen / Q000032:analysis; D011480:Protease Inhibitors / Q000097:blood*; D012217:Rheumatoid Factor / Q000032:analysis; D015842:Serine Proteinase Inhibitors; D000515:alpha 1-Antitrypsin / Q000032:analysis; D000511:alpha-Macroglobulins / Q000032:analysis
D001798:Blood Proteins; D010446:Peptide Fragments; D011480:Protease Inhibitors; D015842:Serine Proteinase Inhibitors; D000515:alpha 1-Antitrypsin; D000511:alpha-Macroglobulins; D000990:Antithrombin III; D010958:Plasminogen; D012217:Rheumatoid Factor