Given the current downward trend in energy consumption among the majority of the population, it becomes obvious that an adequate intake of micronutrients from a regular diet is theoretically impossible, even with the usual need for them. Accordingly, in situations accompanied by an increase in the need for micronutrients, their deficiency becomes all the more obvious, leading to a sharp decrease in human resistance to the effects of adverse environmental factors. The most common clinical sign of zinc deficiency is skin changes (hyperkeratosis, parakeratosis, acrodermatitis). Zinc deficiency is the basis of enteropathic acrodermatitis, an autosomal recessive disease, the clinical picture of which is characterized by the appearance of grouped blisters on the skin in the elbow and knee joints, distal extremities and around natural openings in people suffering from gastrointestinal diseases. The contents of the blisters are usually serous or purulent. Along with these changes, there may be alopecia, nail changes, blepharitis, stomatitis. Other manifestations of zinc deficiency are: growth retardation, gonadal atrophy, disorders of spermatogenesis, mental disorders. Zinc deficiency is also characterized by growth retardation and delayed puberty in adolescents, hypogonadism in men, decreased appetite, delayed wound healing, taste changes, and impaired dark adaptation. In moderate cases of zinc deficiency, oligospermia is observed. Zinc is one of the main trace elements that have a significant effect on the immune system. It has been established that zinc is present in the epithelial cells of the thymus, and its ions in cell culture are able to restore a reduced immunological status, the suppression of which occurs against the background of its deficiency. As a rule, this is clinically manifested by an increase in the frequency of infectious diseases. Zinc deficiency in humans is accompanied by a decrease in the mass of lymphoid tissue (thymus, lymph nodes, spleen, tonsils). People living in zinc-deficient territories are characterized by a decrease in the concentration of zinc in lymphocytes, a decrease in the total number of leukocytes and lymphocytes, and a decrease in the relative and absolute number of Tlymphocytes. There is evidence regarding the effect of zinc on phagocytosis and NK cell activity. It has been established that zinc deficiency leads to a violation of phagocytic function, and an increase in its consumption is accompanied by an increase in the number of peritoneal macrophages and an increase in their phagocytic activity, an increase in the relative content of NK cells. Zinc deficiency is mainly associated with quantitative and functional insufficiency of T-lymphocytes. It has been established that zinc is absolutely necessary for the normal formation of a subpopulation of T-helper cells. In zinc-deficient mice, there is even a thinning of the cortical layer of the thymus due to a decrease in the proliferation of T-helper cells. In people living in zinc-deficient territories, there is also a predominant decrease in the number of cells with a helper phenotype while maintaining the relative content of Suppressors. As a result, against the background of insufficient zinc intake, there is a decrease in the ratio of CD4+/CD8+ lymphocytes. An increase in zinc in the diet of children leads to an increase in the content of CD3+ and CD4+ lymphocytes with an increase in the ratio of CD4+/CD8+. In an experiment on zinc-deficient rats, it was shown that when the zinc level in the body is restored, there is a positive trend in the delayed-type hypersensitivity reaction (HRT), which is statistically significant. Zinc stimulates the production of IL-2. The effect of zinc on humoral immunity is ambiguous. There are experimental data indicating both its negative effect on antibody formation and an increase in IgM and IgG production. It was found that low concentrations of zinc stimulate the proliferation of B-lymphocytes, and its serum level in healthy people correlates with the level of CD19+ lymphocytes. Zinc administration to mice leads to a significant increase in antibody-forming cells (AOC) in the spleen of mice immunized with sheep erythrocytes and increased functional activity in the reaction of blast transformation of lymphocytes with phytohemagglutinins (RBTL with PHA). It has been shown that the serum zinc level in patients with atopic allergies is lower than in healthy individuals. At the same time, there is evidence of a positive effect on the course of allergies from the use of medium doses of zinc during the first 6 months of children’s life. A sharp decrease in zinc content was noted in frequently ill children. Zinc deficiency contributes to the spread of infection and exacerbation of diabetes, AIDS, kidney failure, alcoholic liver cirrhosis and cancer. There are few data on the clinical manifestations of selenium deficiency. It is believed that it is manifested by a decrease in anti-infective immunity and, consequently, an increase in the frequency of colds (mainly viral) and inflammatory diseases, cardiomyopathy, decreased thyroid function, growth retardation, skin lesions (dermatitis, eczema), hair changes (loss, weak growth) and nails (dystrophy). Against the background of selenium deficiency, liver dysfunction (decreased protein-synthesizing and detoxification functions), hypercholesterolemia, glaucoma and cataracts are noted. Low selenium status is associated with an increase in the frequency and severity of viral diseases, and an increase in the virulence of viruses. Selenium deficiency is accompanied by impaired phagocytosis, however, it has been shown that high doses of selenium cause a significant decrease in cytotoxicity of peritoneal macrophages. The relative number of NK cells depends on the content of selenium in the serum. The fact that selenium is able to stimulate the function of these cells is evidenced by its ability to significantly reduce mortality in mice infected with the Coxsackie virus. A correlation was found between the plasma concentration of selenium and the content of CD4+ lymphocytes (P<0.01). An increase in selenium intake leads to an increase in their activity, an increase in the number of IL-2 receptors on them, and an improvement in the migration ability of lymphocytes. There is an increase in delayed-onset hypersensitivity reaction (HRT) in the experiment. It has been found that increased selenium intake stimulates the humoral immune response. Clinical signs of iron deficiency: hypochromic anemia, increased fatigue and mild excitability, headaches, myoglobin-deficient myocardiopathy; atrophic glossitis, gingivitis, cheilitis; dryness of the mucous membrane of the mouth and tongue; atrophic gastritis, gastric dyspepsia; decreased resistance to infections. With iron deficiency, bactericidal activity and myeloperoxidase activity of neutrophil granulocytes decrease. Examination of elderly patients revealed a significant dependence of NK cell activity on serum ferritin levels. In children with iron deficiency, there is a decrease in circulating T-lymphocytes and the proliferative response of lymphocytes to mitogens. They also have a decrease in the concentration of IL-2 and IL-6 in the blood serum. At the same time, there is evidence that the administration of high doses of the same drug to patients with infectious diseases increases the severity of infection and increases the frequency of deaths. Source: elibrary.ru