Info

Type

Donor

Example

Isograft

Identical twin

Bone marrow transplant from a healthy twin to a twin who has leukemia

Autograft

Self

Skin graft from one part of body to replace burned skin

Allograft

Same species

Kidney transplant from relative or closely matched donor

Xenograft Different species

Heart valves from a pig

in autoimmune hemolytic anemia, autoantibodies destroy red blood cells. In autoimmune ulcerative colitis, colon cells are the target, and severe abdominal pain results. Table 16.10 lists some autoimmune disorders.

Why might the immune system attack body tissues? Perhaps a virus, while replicating within a human cell, "borrows" proteins from the host cell's surface and incorporates them onto its own surface. When the immune system "learns" the surface of the virus to destroy it, it also learns to attack the human cells that normally bear the particular protein. Another explanation of autoimmu-nity is that somehow T cells never learn in the thymus to distinguish self from nonself.

A third possible route of autoimmunity is when a nonself antigen coincidentally resembles a self antigen. This may explain type I diabetes, which is a deficiency of insulin, the hormone required to transport glucose from the blood into cells that use it (see Clinical Application 13.4). Type I diabetes strikes 1 in 500 people under the age of twenty—they must inject insulin several times a day.

Part of a protein on insulin-producing cells matches part of bovine serum albumin (BSA), which is a protein in cow's milk. Perhaps children with an allergy to cow's milk develop antibodies against BSA, which later attack the similar-appearing pancreas cells, causing type I diabetes. An ongoing study is tracking the health of children with family histories of type I diabetes who have avoided drinking cow's milk, compared to similarly high-risk children who have drunk cow's milk.

Some disorders traditionally thought to be autoimmune in origin may in fact have a more bizarre cause— fetal cells persisting in a woman's circulation, even decades after the fetus has grown up! In response to an as yet unknown trigger, the fetal cells, perhaps "hiding" in

Disorder

Symptoms

Antibodies Against

Glomerulonephritis

Lower back pain

Kidney cell antigens that resemble streptococcal bacteria antigens

Graves disease

Restlessness, weight loss, irritability, increased heart rate and blood pressure

Thyroid gland antigens near thyroid-

stimulating hormone receptor, causing overactivity

Type I diabetes

Thirst, hunger, weakness, emaciation

Pancreatic beta cells

Hemolytic anemia

Fatigue and weakness

Red blood cells

Myasthenia gravis

Muscle weakness

Receptors for neurotransmitters on skeletal muscle

Pernicious anemia

Fatigue and weakness

Binding site for vitamin B on cells lining stomach

Rheumatic fever

Weakness, shortness of breath

Heart valve cell antigens that resemble streptococcal bacteria antigens

Rheumatoid arthritis

Joint pain and deformity

Cells lining joints

Systemic lupus erythematosus

Red rash on face, prolonged fever, weakness, kidney damage

DNA, neurons, blood cells

Ulcerative colitis

Lower abdominal pain

Colon cells

Figure

Scleroderma hardens the skin. Some cases appear to be caused by a long-delayed reaction of the immune system to cells retained from a fetus—even decades earlier.

Figure

Scleroderma hardens the skin. Some cases appear to be caused by a long-delayed reaction of the immune system to cells retained from a fetus—even decades earlier.

a tissue such as skin, emerge, stimulating antibody production. If we didn't know the fetal cells were there, the resulting antibodies and symptoms would appear to be an autoimmune disorder. This mechanism, called mi-crochimerism ("small mosaic"), may explain the higher prevalence of autoimmune disorders among women. It was discovered in a disorder called scleroderma, which means "hard skin" (figure 16.25).

Patients describe scleroderma, which typically begins between ages 45 and 55, as "the body turning to stone." Symptoms include fatigue, swollen joints, stiff fingers, and a masklike face. The hardening may affect blood vessels, the lungs, and the esophagus, too. Clues that scleroderma is a delayed response to persisting fetal cells include the following observations:

• It is much more common among women.

• Symptoms resemble those of graft-versus-host disease (GVHD), in which transplanted tissue produces chemicals that destroy the body. Antigens on cells in scleroderma lesions match those involved in GVHD.

• Mothers who have scleroderma and their sons have cell surfaces that are more similar than those of unaffected mothers and their sons. Perhaps the similarity of cell surfaces enabled the fetal cells to escape surveillance and destruction by the woman's immune system. Female fetal cells probably have the same effect, but this is more difficult to demonstrate because these cells cannot be distinguished from maternal cells by the presence of a Y chromosome.

It's possible that other disorders traditionally considered to be autoimmune may actually reflect an immune system response to lingering fetal cells.

Chronic fatigue syndrome is a poorly understood immune system imbalance. The condition begins suddenly, producing fatigue so great that getting out of bed is an effort. Chills, fever, sore throat, swollen glands, muscle and joint pain, and headaches are also symptoms. The various disabling aches and pains reflect an overactive immune system. Affected people have up to forty times the normal amount of interleukin-2 and too many cytotoxic T cells, yet too little interferon. It is as if the immune system mounts a defense and then doesn't know when to shut it off. The cause of chronic fatigue syndrome is not known.

How are allergic reactions and immune reactions similar yet different?

How does a tissue rejection reaction involve an immune response?

How is autoimmunity an abnormal functioning of the immune response?

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