ALFRED D. STEINBERG, M.D.; ELIZABETH S. RAVECHÉ, Ph.D.; CARL A. LASKIN, M.D.; HOWARD R. SMITH, M.D.; THOMAS SANTORO, M.D.; MICHAEL L. MILLER, M.D.; PAUL H. PLOTZ, M.D.
Systemic lupus erythematosus is a multisystem, antibody-mediated, autoimmune disorder that occurs spontaneously in humans and mice. Genetic factors appear to play an important predisposing role in the disorder: The presence of certain genes may produce a generalized immune abnormality, whereas others may lead to specific autoantibodies. Environmental triggers increase autoantibody production and augment the expression of illness. Bacterial and viral illnesses can provide stimulation by activating macrophages and T cells that, in turn, stimulate B cells. In the absence of normal control mechanisms, the stimulatory process is not suppressed, and excessive stem cell proliferation results in abnormal B-cell proliferation. A trigger for the disease is the signaling of the proliferating B cells to differentiate into antibody-forming cells. Most autoantibody-producing B cells can be eliminated from mice with lupus erythematosus by virtue of the presence of the gene, xid. In addition, administration of an analog of arachidonic acid is an effective treatment for murine lupus erythematosus.
ALFRED D. STEINBERG, ELIZABETH S. RAVECHÉ, CARL A. LASKIN, HOWARD R. SMITH, THOMAS SANTORO, MICHAEL L. MILLER, et al. Systemic Lupus Erythematosus: Insights from Animal Models. Ann Intern Med. 1984;100:714–727. doi: 10.7326/0003-4819-100-5-714
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Published: Ann Intern Med. 1984;100(5):714-727.
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