Open AccessIdentification of polyclonal and monoclonal antibodies against tissue plasminogen activator in the antiphospholipid syndrome
Author(s) -
Lu CaiSheng,
Horizon Arash A.,
Hwang KwanKi,
FitzGerald John,
Lin WeiShiang,
Hahn Bevra H.,
Wallace Daniel J.,
Metzger Allan L.,
Weisman Michael H.,
Chen Pojen P.
Publication year - 2005
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.21485
Subject(s) - plasmin , monoclonal antibody , tissue plasminogen activator , polyclonal antibodies , t plasminogen activator , monoclonal , medicine , immunology , fibrin , plasminogen activator , fibrinolysis , antibody , microbiology and biotechnology , chemistry , biochemistry , biology , enzyme
Abstract Objective To test the hypotheses that some plasmin‐reactive anticardiolipin antibodies (aCL) may bind to tissue plasminogen activator (tPA) and that some of the tPA‐reactive aCL may inhibit tPA activity. Methods We studied the reactivity of 8 patient‐derived monoclonal aCL with tPA and examined the presence of IgG anti‐tPA antibodies in patients with the antiphospholipid syndrome (APS). The effects of the reactive monoclonal aCL on the activity of tPA were also examined. Results Six patient‐derived plasmin‐reactive monoclonal aCL bound to tPA. Analysis of plasma samples revealed that 10 of 80 APS patients (12.5%) and 1 of 81 systemic lupus erythematosus patients (1.2%) had antibodies against fibrin‐associated tPA, based on a cutoff value equal to the mean + 2SD of the level in 28 normal subjects. Of the 6 tPA‐reactive monoclonal aCL, 2 of them (CL1 and CL15) inhibited tPA activity. Conclusion Some of the plasmin‐reactive aCL in APS patients may bind to tPA. Of the tPA‐reactive aCL, some (such as CL1 and CL15) may inhibit tPA activity and, thus, may be prothrombotic in the host.