T-lymphocyte subsets and interleukin-2 production in zinc-deficient rats

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Abstract
1. 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.