Regeneration of T-cell helper function in zinc-deficient adult mice

Abstract

Diets deficient in Zn caused rapid atrophy and the thymus and loss of T[thymus-derived]-cell helper function in the young adult A/J mouse. Because Zn deficiency and other nutritional deficiencies cause extensive damage to the immune system, Zn-deficient mice may repair the thymus and fully regenerate T cell helper function if returned to diets containing adequate amounts of Zn. Five wk old A/J female mice were fed a Zn-deficient (< 1 .mu.g of Zn/g) or a Zn-adequate (50 .mu.g of Zn/g) diet for 31 days. Histological examination of thymuses from the Zn-deficient mice revealed that the cortex was preferentially involuted and the thymus was about 1/3 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 (Jerne plaque assay). After the deficient mice were fed a Zn-adequate diet for 1 wk, their response was nearly normal, except that the indirect response was 68% of controls; in this same period, the thymuses of these mice quadrupled in size and exhibited a greatly enlarged cortex repopulated with immature thymocytes. By 2 wk, the thymuses of the previously Zn-deficient mice were normal in size and appearance; however, there was a slight increase in numbers of indirect plaque-forming cells. By 4 wk, the thymus wt, 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 Zn deficiency were able to fully reconstruct the thymus and regenerate T cell helper function. The Zn-deficient young adult mouse can fully restore T-cell-dependent antibody-mediated responses upon nutritional repletion.