LACK OF SUPPRESSIVE ANTIBODY-ACTIVITY IN SERA FROM PATIENTS WITH ACTIVE-PHASE AUTOIMMUNE-DISEASES

Citation
J. Melero et al., LACK OF SUPPRESSIVE ANTIBODY-ACTIVITY IN SERA FROM PATIENTS WITH ACTIVE-PHASE AUTOIMMUNE-DISEASES, Autoimmunity (Print), 28(1), 1998, pp. 47-56
Citations number
26
Categorie Soggetti
Immunology
Journal title
ISSN journal
08916934
Volume
28
Issue
1
Year of publication
1998
Pages
47 - 56
Database
ISI
SICI code
0891-6934(1998)28:1<47:LOSAIS>2.0.ZU;2-1
Abstract
To investigate the presence of a suppressive antibody activity in sera from patients: with autoimmune diseases, the IgG autoreactivity in wh ole serum was compared to that of the IgG fraction purified by affinit y chromatography on protein G-sepharose. Competitive inhibition assays on the binding to histone, dsDNA, RNP and thyroglobulin of the purifi ed IgG fraction by the autologous IgM present in serum without IgG and depleted of < 100 kD components (named IgM fraction) were also perfor med. The IgG reactivity to the autoantigens tested was considerably in creased in the IgG fraction than in the whole serum drawn from a healt hy control and from three SLE patients in an inactive-phase of disease . Addition of the IgM fraction to the autologous purified IgG resulted in a dose-dependent inhibition of IgG binding to the autoantigens tes ted. However, no differences were observed between the autoreactivity of the IgG in whole serum and that of the purified IgG fraction from a ctive-phase SLE patients, or fr om two patients with autoimmune thyroi ditis, and the autologous IgM fractions did not inhibit significantly binding to the autoantigens under study of the purified IgG fraction. Our findings support the concept that the IgG autoreactivity in physio logical conditions is regulated by idiotypic interactions between IgG and IgM, and suggest that this regulation is broken in the active phas e of autoimmune diseases and that clinical remission from SLE could be associated with the restoration of this control mechanism. Additional ly, qualitative differences, such as polyreactivity or change of idiot ype in the autoreactive IgG fraction from active-phase disease might c ontribute to escape of regulation.