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Diets deficient in zinc cause rapid atroph of the thymus and loss of T-cell helper function in e yougadun t A/J mouse. Because zinc deficiency, as well as other nutritional deficiencies, causes extensive damage to the immune system, the question arose as to whether zinc deficient mice could repair the thymus and fully regenerate T-cell helper function if returned to diets containing adequate amounts of zinc. Fiveweek-old A/J female mice were fed either a zinc-deficient (<1 ,ug of Zn per g) or a zinc-adequate (50°,g of Zn per g) diet for 31 days. Histological examination of thymuses from the zinc-deficient mice revealed that the cortex was preferentially involuted and the thymus was about one-third of normal size. The direct plaque-forming cells produced per mouse spleen in response to immunization with sheep erythrocytes was 34% of normal; indirect plaque-forming cells were 18% of normal plaque assay). After the deficient mice had been fed a zin-adequate diet for 1 week, their response was nearl normal, except that the indirect response was 68% of controls; in this same period, the thymuses of these mice had quadrupled in size and exhibited a greatly Enlarged cortex repopulated with immature thymocytes. By 2 weeks, the thymuses of the previously zinc-deficient mice were normal in size and appearance; however, there was a slight increase in numbers of indirect plaque-forming cells. By 4 weeks, the thymus weights, direct and indirect plaque-forming cell counts, and secondary response of the previously deficient mice were normal. Mice that were nearly athymic after 45 days of dietary zinc deficiency were also able to fully reconstruct the thymus and regenerate T-cell helr function. The data show that the zinc-deficient oung ult mouse has the capacity to fully restore the T-cefldependent antibody-mediated responses upon nutritional repletion. It has been known for some time that malnourished children are more susceptible to disease and infection (1, 2) and that the death rate from ordinary childhood diseases is extraordinarily high among these children compared to their normal counterparts (3). From available clinical data it is apparent that rapid atrophy of the thymus is a feature common to many types of deficiencies as shown by autopsies performed on children who suffered from protein-calorie malnutrition, kwashiorkor, or marasmus (4, 5). Laboratory animals made deficient in certain amino acids (6), vitamins (7), or trace elements (8) The severity of the loss of iune function and the swiftness with which zinc deficiency brought about destruction of the thymus brought to the fore the question of repair. Do nutritionally deficient animals have the capacity to repair damaged immune systems if re-fed nutritionally adequate diets and is there full restoration of immune function? Little information is available in the literature (10) on the ability of nutritionally deficient humans or animals to repair lymphocyte functions upon nutritional repletion. The question of repair capacity is of obvious importance to...

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