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Immunology and Transplants
Understanding the Immune System

Adapted by Mary Shomon

Since organ transplantation was introduced over a quarter of a century ago, it has become a widespread remedy for life-threatening disease. Several thousand kidney transplants are performed each year in the United States alone. In addition, physicians have succeeded in transplanting the heart, lungs, liver and pancreas.

The success of a transplant-whether it is accepted or rejected-depends on the stubbornness of the immune system. For a transplant to "take," the body of the recipient must be made to suppress its natural tendency to get rid of foreign tissue.

Scientists have tackled this problem in two ways. The first is to make sure that the tissue of the donor and the recipient are as similar as possible. Tissue typing, or histocompatibility testing, involves matching the markers of self on body tissues; because the typing is usually done on white blood cells, or leukocytes, the markers are referred to as human leukocyte antigens (HLA). Each cell has a double set of six major antigens, designated HLA-A, B, C, and three types of HLA-D-DR, DP, and DQ. (HLA-A, B, and C are the same as the class I antigens encoded by the genes of the major histocompatibility complex; HLA-D region molecules are the class II MHC antigens.)

Each of the HLA antigens exist-in different individuals-in as many as 20 varieties, so that the number of possible HLA types reaches about 10,000. Histocompatibility testing relies on antibodies to determine if a potential organ donor and recipient share two or more HLA antigens, and thus are likely to make a good "match." The best matches are identical twins; next best are close relatives, especially brothers and sisters.

The second approach to taming rejection is to lull the recipient's immune system. This can be achieved through a variety of powerful immunosuppressive drugs. Steroids suppress lymphocyte function; the drug cyclosporine holds down the production of the lymphokine interleukin-2, which is necessary for T cell growth. When such measures fail, the graft may yet be saved with a new treatment: OKT3 is a monoclonal antibody that seeks out the T3 marker carried on all mature T cells. By either destroying T cells or incapacitating them, OKT3 can bring an acute rejection crisis to a halt.

Not surprisingly, any such all-out assault on the immune system leaves a transplant recipient susceptible to both opportunistic infections and lymphomas. Although such patients need careful medical followup, many of them are able to lead active and essentially normal lives.

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