Abstract

The relationship between sex hormones and immunological processes is well documented. Women are known to have higher immunoglobulin levels than men, a higher incidence of immunologically based illnesses, and the ability to mount a more vigorous immune response to infections. Both cell-mediated immunity and natural killer cell activity are diminished during pregnancy and menopausal women have an increased release of interleukin-1 by monocytes, which is reversible by hormone replacement therapy. Depending on dose, estrogens may act as immunosuppressors or immunostimulants. Estrogen administered before bone marrow transplantation has been shown to result in increased graft failure. The mixed lymphocyte reaction is enhanced by estradiol and fluctuating lymphocyte responses are observed during normal menses, pregnancy, and the use of oral contraceptives. As might be expected, pregnancy and the menstrual cycle affect the severity of autoimmune disease. Androgens also affect immune function. Testosterone has been shown to suppress anti-DNA antibody production in peripheral blood mononuclear cells from patients with systemic lupus erythematosus (SLE), and graft rejection in rodents is delayed by injection of testosterone. Progesterone is an immunosuppressive agent, and may be the basis for the gender gap in the disease SLE. It is possible that genes related to autoimmunity may be hormonally regulated, although there is no direct evidence for this. Given these data it is hardly surprising to find that many gender related differences exist in the arena of organ transplantation. This chapter discusses these differences as they relate to organ failure, and liver, kidney, and pancreas transplantation.

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