Autoantibodies within families of patients with systemic lupus erythematosus are not directed against the same nuclear antigens

• Published in: Journal of rheumatology Vol. 28; no. 2; pp. 284 - 287
• Main Authors: VAN DER LINDEN, Michiel W, WESTENDORP, Rudi G. J, ZIDANE, Majida, MEHEUS, Lydie, HUIZINGA, Tom W. J
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Toronto, ON The Journal of Rheumatology 01-02-2001; Journal of Rheumatology Publishing
• Subjects: Adult; Antibodies, Antinuclear - genetics; Antibodies, Antinuclear - immunology; B-Lymphocytes - immunology; Biological and medical sciences; Female; Humans; Lupus Erythematosus, Systemic - genetics; Lupus Erythematosus, Systemic - immunology; Lupus Erythematosus, Systemic - physiopathology; Male; Medical sciences; Nuclear Proteins - genetics; Nuclear Proteins - immunology; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; Human; Immunopathology; Connective tissue disease; Skin disease; Immune response; Antibody; Family study; Pathogenesis; Cell nucleus; Autoantibody; Autoimmune disease; B-Lymphocyte; Immunological method; Systemic disease; Genetics; Lupus erythematosus; Disseminated; ELISA assay; Humoral immunity
• ISSN: 0315-162X; 1499-2752

OBJECTIVE: The presence of antinuclear autoantibodies in systemic lupus erythematosus (SLE) is influenced by genetic factors.
The presence of autoantibodies in healthy family members of patients has been reported. Our hypothesis was that autoantibodies
are directed against the same antigens in first-degree family members of patients with SLE as in their patient relative. METHODS:
Plasma was harvested from 50 patients with SLE, 154 unaffected first-degree family members, and 330 healthy controls. Presence
of autoantibodies against 14 specific nuclear antigens was tested by the ELISA based line immunoassay INNO-LIA method. RESULTS:
Seventy-four percent of patients, 32% of first-degree family members, and 1.5% of healthy controls had antibodies against
any nuclear antigen. Most frequent autoantibodies in the patients were anti-histone and anti-SSA, whereas in the family members
these were anti-RNP-C and anti-Topo-I/Scl. Presence and specificity of autoantibodies in family members were independent of
the presence or absence of that autoantibody in their patient relative (chi-square p > 0.1 for all 14 antigens). CONCLUSION:
Autoantibodies in family members and their patient relatives are not directed against the same nuclear antigens. Thus a familial
aspecific dysfunction of the B lymphocyte is the most likely explanation for autoantibody production in SLE.