DNA receptor dysfunction in systemic lupus erythematosus and kindred disorders. Induction by anti-DNA antibodies, antihistone antibodies, and antireceptor antibodies

Robert (Rob) Bennett, B. L. Kotzin, M. J. Merritt

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    Abstract

    The ability of sera from patients with SLE and similar connective tissue diseases to induce dysfunction of the receptor for DNA was studied. All SLE and MCTD sera studied resulted in marked inhibition of DNA receptor binding. Furthermore, the sera from a subgroup of patients with other rheumatic diseases and a surprisingly high percentage of asymptomatic relatives of SLE patients exhibited a similar effect. The humoral factors causing this defect were shown to be of at least three reactivities: (a) antibodies to DNA, (b) antibodies to histones, and (c) antibodies to the DNA receptor itself. The reactivity of anti-DNA antihistone antibodies is dependent upon intact cell-surface DNA, and reconstitution experiments suggest that antihistone antibodies are reactive with histones complexed to this DNA, which in turn is bound to the DNA receptor. Cells with an antibody-induced DNA receptor defect are unable to bind DNA; the subsequent inability to degrade DNA may have important consequences in diseases such as SLE in which DNA-anti-DNA immune complexes are of pathogenetic significance.

    Original languageEnglish (US)
    Pages (from-to)850-863
    Number of pages14
    JournalJournal of Experimental Medicine
    Volume166
    Issue number4
    StatePublished - 1987

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    Antinuclear Antibodies
    Systemic Lupus Erythematosus
    Antibodies
    DNA
    Histones
    Serum
    Mixed Connective Tissue Disease
    Aptitude
    Connective Tissue Diseases
    DNA receptor
    Antigen-Antibody Complex
    Rheumatic Diseases

    ASJC Scopus subject areas

    • Immunology

    Cite this

    DNA receptor dysfunction in systemic lupus erythematosus and kindred disorders. Induction by anti-DNA antibodies, antihistone antibodies, and antireceptor antibodies. / Bennett, Robert (Rob); Kotzin, B. L.; Merritt, M. J.

    In: Journal of Experimental Medicine, Vol. 166, No. 4, 1987, p. 850-863.

    Research output: Contribution to journalArticle

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