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Biological Trace Element Research

, Volume 30, Issue 3, pp 233–244 | Cite as

In vitro OKT3-induced mitogenesis in selenium-deficient patients on a diet for phenylketonuria

  • R. J. Collins
  • P. J. Boyle
  • A. E. Clague
  • A. E. Barr
  • S. C. Latham
Article

Abstract

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.

Index Entries

T-Lymphocyte activation and proliferation OKT3 mitogenesis selenium phenylketonuria 

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Copyright information

© Humana Press Inc. 1991

Authors and Affiliations

  • R. J. Collins
    • 1
  • P. J. Boyle
    • 1
  • A. E. Clague
    • 2
  • A. E. Barr
    • 2
  • S. C. Latham
    • 3
  1. 1.Division of Immunology, Department of PathologyRoyal Brisbane HospitalHerstonAustralia
  2. 2.Division of Chemical Pathology, Department of PathologyRoyal Brisbane HospitalHerstonAustralia
  3. 3.Department of MedicineRoyal Children's HospitalHerstonAustralia

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