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Figure 20-6. Characteristic "butterfly" rash over the cheeks of a young girl with SLE.

Several proposed mechanisms for the induction of SLE are discussed below, yet a clear picture of the causes of SLE is not yet elucidated.

 Systemic Lupus Erythematosus (SLE) is characterized by fever, weakness, arthritis, skin rashes (see figure at left), pleurisy, and kidney dysfunction. Affected individuals may produce autoantibodies to a range of tissue antigens such as DNA, histones, RBCs, platelets, leukocytes, and clotting factors. SLE typically appears in women between 20 and 40 years of age with a female:male ratio of 10:1.

An example of complications arising from SLE is when immune complexes of autoantibodies and various nuclear antigens are deposited along the walls of small blood vessels. This deposition activates the complement system, resulting in glomerulonephritis and damage to the blood-vessel wall (vasculitis). This blood vessel damage can lead to widespread tissue damage.
Proposed Mechanisms of SLE
Inappropriate expression of class II MHC molecules, which are normally expressed only on antigen-presenting cells, may serve to sensitize TH cells to peptides derived from inappropriate cells, allowing activation of B cells of TC cells or sensitization of TDTH cells against self-antigen. There is also evidence that suggests that certain molecules can induce inappropriate class II MHC expression. IFN-g is one of the agents shown to have this effect on a wide variety of cells. This is relevant to SLE because patients with active disease have been shown to have higher serum titers of IFN-g than patients with inactive disease.
A number of viruses and bacteria can produce nonspecific polyclonal B-cell activation, inducing the proliferation of numerous clones of B cells that express IgM in the absence of TH cells. If B cells reactive to self-antigens are activated by this mechanism, autoantibodies can appear. Lymphocytes from patients with SLE produce large quantities of IgM, suggesting that they have been polyclonally activated.
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Figure 20-9. Autoimmune mechanisms and disorders
Figure 20-7. Multiple Sclerosis
Figure 20-5. Myasthenia Gravis
Figure 20-4. Graves' Disease
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© Created by Duane W. Sears & UCSB student, Natasha Marston
March 20, 1998