Zinc deficiency causes acrodermatitis enteropathica, alopecia, impaired wound healing, and immune dysfunction. The molecular explanation for zinc's role in immune function involves:

• A Zinc is required for the folded structure of zinc finger transcription factors including those regulating lymphocyte differentiation (p53, thymulin, nuclear receptors) ✓
• B Zinc is an essential cofactor for superoxide dismutase (Cu/Zn-SOD) only in granulocytes
• C Zinc inhibits myeloperoxidase, reducing neutrophil oxidative burst
• D Zinc is incorporated into cytochrome c oxidase in lymphocyte mitochondria

Explanation

Zinc has multiple immunological roles. Zinc finger motifs (Cys2His2 and Cys4 types) are structural domains in hundreds of transcription factors, including those governing lymphocyte development (Ikaros, GATA-3), p53, retinoic acid receptors (RARs), and thymulin (a thymic peptide hormone requiring zinc for activity). Without adequate zinc, these zinc finger proteins lose structural integrity and DNA-binding capacity, impairing T-cell maturation, cytokine production, and NK cell activity. Thymulin, requiring zinc for activity, is necessary for T-cell differentiation in the thymus—its inactivity in zinc deficiency contributes to the T-cell lymphopenia observed. Cu/Zn-SOD deficiency is a secondary consequence but not the primary immune mechanism, and zinc does not inhibit myeloperoxidase.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

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Written and medically reviewed by the StethoPrep medical team.