I. It has been suggested that zinc-deficiency impairs cellular (T-lymphocyte-mediated) immune responses via a selective effect on helper T-lymphocytes. We have addressed this question in the rat by employing recently developed reagents in the form of monoclonal antibodies which specifically identify rat T-lymphocyte subsets (identifying total T-cells, helper T-cells and suppressor T-cells) and also by quantifying helper T-cell function by measurement of the helper T-cell-derived molecule interleukin-2 (IL-2).2. Zn-deficiency induced T-cell atrophy (assessed morphologically and phenotypically with anti-rat T-cell monoclonal antibodies) in both peripheral blood and spleen. The use of these specific monoclonal antibodies failed to demonstrate a selective effect of Zn deficiency on the helper T-cell fraction of the total T-lymphocyte population.3. In contrast, the results of functional assays of the T-lymphocyte response were dependent on the conditions of culture but suggested that the generation of IL-2 and its corresponding receptor were determined by the intracellular Zn status. Thus, in vivo, helper T-lymphocyte numbers are non-specifically reduced since other T-cell subsets are also reduced in response to appropriate stimulation. The functional consequences of this are dependent on the intracellular concentration of Zn but appear to influence both IL-2 production and its receptors on activated T-cells.

1. The interrelations between nutritional and ccllular immune function measurements were studied in seventy patients suffering from various degrees of malnutrition. They included patients with liver disease, inflammatory bowel disease, neoplastic disease, neurological patients, post-operative surgical patients and patients with respiratory problems.2. Nutritional measurements included: anthropometry, serum proteins, various vitamins and trace elements, and a prognostic nutritional index (PNI) was calculated.3. Immunological measurements included: ( I ) natural killer (NK) cell activity, (2) antibody-dependent cellular cytotoxicity (ADCC), (3) lymphocyte proliferation in response to the mitogens concanavalin A (Con A), phytohaemagglutinin (PHA) and pokeweed mitogen (PWM) in both AB and autologous serum.4. There was no association between anthropometric measurements and tests of immune function. 5. The lymphocyte proliferation in response to mitogenic stimulation in the malnourished patients was depressed in autologous serum compared with the response of the same lymphocytes in pooled AB serum. The lymphocyte proliferation in response to Con A correlated with transferrin in autologous serum (r 0.46, n 49, P < 0.0 I ) and to a lesser extent in AB serum (r 0.33, n 51, P < 0.05). There was a difference in the Con A-stimulated tritiated-thymidine uptake between patients with low and normal serum zinc levels (P < 0.05) for cultures performed in autologous serum, but not AB serum.6. There was a significant correlation between NK cell activity and vitamin C (r 0.43, n 60, P < 0.01). There was no relation between nutritional measurements and ADCC or the lymphocyte response to stimulation with PHA or PWM.7. The results suggest that the severity of overall malnutrition does not influence several different aspects of the cellular immune response. However, the results do suggest that certain individual nutrients, particularly vitamin C and Zn, do influence the immunoreactivity of different lymphocyte subpopulations.

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