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The damage and pathology of systemic lupus erythematosus (SLE) is caused by type III hypersensitivity reactions. Autoantibodies produced in SLE are directed against nuclear and cytoplasmic proteins. Anti-nuclear antibodies (ANAs) are present in more than 95% of patients with SLE, C.C. Mok, C.S. Lau. “Pathogenesis of Systemic Lupus Erythematosus.” Journal of Clinical Pathology 56 no. 7 (2003):481—490. with additional autoantibodies including anti-double–stranded DNA (ds-DNA) and anti-Sm antibodies (antibodies to small nuclear ribonucleoprotein). Anti-ds-DNA and anti-Sm antibodies are unique to patients with SLE; thus, their presence is included in the classification criteria of SLE. Cellular interaction with autoantibodies leads to nuclear and cellular destruction, with components released after cell death leading to the formation of immune complexes.
Because autoantibodies in SLE can target a wide variety of cells, symptoms of SLE can occur in many body locations. However, the most common symptoms include fatigue, fever with no other cause, hair loss, and a sunlight-sensitive "butterfly" or wolf-mask (lupus) rash that is found in about 50% of people with SLE ( [link] ). The rash is most often seen over the cheeks and bridge of the nose, but can be widespread. Other symptoms may appear depending on affected areas. The joints may be affected, leading to arthritis of the fingers, hands, wrists, and knees. Effects on the brain and nervous system can lead to headaches, numbness, tingling, seizures, vision problems, and personality changes. There may also be abdominal pain, nausea, vomiting, arrhythmias, shortness of breath, and blood in the sputum. Effects on the skin can lead to additional areas of skin lesions, and vasoconstriction can cause color changes in the fingers when they are cold (Raynaud phenomenon). Effects on the kidneys can lead to edema in the legs and weight gain. A diagnosis of SLE depends on identification of four of 11 of the most common symptoms and confirmed production of an array of autoantibodies unique to SLE. A positive test for ANAs alone is not diagnostic.
[link] summarizes the causes, signs, and symptoms of select autoimmune diseases.
| Select Autoimmune Diseases | ||
|---|---|---|
| Disease | Cause | Signs and Symptoms |
| Addison disease | Destruction of adrenal gland cells by cytotoxic T cells | Weakness, nausea, hypotension, fatigue; adrenal crisis with severe pain in abdomen, lower back, and legs; circulatory system collapse, kidney failure |
| Celiac disease | Antibodies to gluten become autoantibodies that target cells of the small intestine | Severe diarrhea, abdominal pain, anemia, malnutrition |
| Diabetes mellitus (type I) | Cytotoxic T-cell destruction of the insulin-producing β cells of the pancreas | Hyperglycemia, extreme increase in thirst and urination, weight loss, extreme fatigue |
| Graves disease | Autoantibodies target thyroid-stimulating hormone receptors, resulting in overstimulation of the thyroid | Hyperthyroidism with rapid and irregular heartbeat, heat intolerance, weight loss, goiter, exophthalmia |
| Hashimoto thyroiditis | Thyroid gland is attacked by cytotoxic T cells, lymphocytes, macrophages, and autoantibodies | Thyroiditis with goiter, cold intolerance, muscle weakness, painful and stiff joints, depression, memory loss |
| Multiple sclerosis (MS) | Cytotoxic T-cell destruction of the myelin sheath surrounding nerve axons in the central nervous system | Visual disturbances, muscle weakness, impaired coordination and balance, numbness, prickling or “pins and needles” sensations, impaired cognitive function and memory |
| Myasthenia gravis | Autoantibodies directed against acetylcholine receptors within the neuromuscular junction | Extreme muscle weakness eventually leading to fatal respiratory arrest |
| Psoriasis | Cytokine activation of keratinocytes causes rapid and excessive epidermal cell turnover | Itchy or sore patches of thick, red skin with silvery scales; commonly affects elbows, knees, scalp, back, face, palms, feet |
| Rheumatoid arthritis | Autoantibodies, immune complexes, complement activation, phagocytes, and T cells damage membranes and bone in joints | Joint inflammation, pain and disfigurement, chronic systemic inflammation |
| Systemic lupus erythematosus (SLE) | Autoantibodies directed against nuclear and cytoplasmic molecules form immune complexes that deposit in tissues. Phagocytic cells and complement activation cause tissue damage and inflammation | Fatigue, fever, joint pain and swelling, hair loss, anemia, clotting, a sunlight-sensitive "butterfly" rash, skin lesions, photosensitivity, decreased kidney function, memory loss, confusion, depression |
The thyroid-stimulating immunoglobulin that acts like thyroid-stimulating hormone and causes Graves disease is an antibody to the ________.
thyroid-stimulating hormone receptor
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