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Demonstration of Electrophoretic Heterogeneity of Serum β 2 ‐Microglobulin in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Evidence against Autoantibodies to β 2 ‐Microglobulin
Author(s) -
PLESNER T.,
WIIK A.
Publication year - 1979
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1979.tb02728.x
Subject(s) - beta 2 microglobulin , rheumatoid arthritis , autoantibody , immunology , immunoelectrophoresis , medicine , antiserum , antibody , chemistry , microbiology and biotechnology , biology
A sensitive crossed radioimmunoelectrophoretic method (CRIE), originally developed to study lymphocyte‐associated β 2 ‐microglobulin (β 2 m), was applied in the study of serum β 2 m in patients with systemic lupus erythemutosus (SLE) and rheumatoid arthritis (RA). In six of seven patients with SLE and nineteen of twenty‐seven patients with RA a considerable elec‐trophoretic heterogeneity of serum β 2 m was found. In addition to the normally seen symmetric β 2 m precipitate, a β 2 precipitate exhibiting complete immunochemical identity was found in the α‐electrophoretic region. Binding of isolated I25 l‐labelled β 2 m to the abnormal precipitate was demonstrated in crossed immunoelectrophoresis. After gel filtration of sera exhibiting the above‐mentioned β 2 m binding, all β 2 m was eluted in low molecular weight fractions corresponding to free β 2 m. By application of appropriate antisera and a glycoprotein‐binding lectin in intermediate gels in CRIE, it was shown that the possible β 2 m‐binding ligand is not an antibody, not a major constituent of normal human serum, and not unmodified HLA alloantigen. The abnormality was not restricted to patients with high disease activity but was found more frequently and was more pronounced (mean score 1.6 arbitrary units against 0.57 arbitrary units, P < 0.01) in such patients. Thus our data exelude the possibility that autoantibodies to β 2 m were present in serum from patients with SLE and RA.