In vitro OKT3-induced mitogenesis in selenium-deficient patients on a diet for phenylketonuria
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- Collins, R.J., Boyle, P.J., Clague, A.E. et al. Biol Trace Elem Res (1991) 30: 233. doi:10.1007/BF02991418
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Patients with phenylketonuria (PKU) are frequently deficient in the essential trace element selenium (Se), because of their very low protein diet. Using two approaches to investigate T-cell response to proliferative signaling, viz, mitogenesis caused by the monoclonal antibody OKT3 and the plant lectin phytohaemagglutinin (PHA), we demonstrated significantly reduced responses to optimal concentrations of OKT3 in a group of PKU patients with reduced serum Se compared with a normal group (p=0.0005) and with a group of PKU patients whose serum Se was normal (p=0.0023). The response of the Se-deficient group to optimal levels of PHA did not differ from that of the normal controls or from that of Se-normal PKU patients. A dose-dependent relationship between serum Se levels and mitogenic response was evident for OKT3 (r=0.34,p=0.0154), but not for PHA (r=−0.02,p=0.9086). We suggest that the reduced response to OKT3 mitogenesis in Se-deficient PKU patients is possibly the consequence of impaired Se-dependent metabolic activity, which affects mitogenic signaling via the T cell antigen receptor (TCR/CD3) complex.