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  Vol. 123 No. 12, December 1987 TABLE OF CONTENTS
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  36TH ANNUAL SYMPOSIUM ON THE BIOLOGY OF SKIN
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Zinc Deficiency and Immune Function

Pamela J. Fraker, PhD; Paula Jardieu, PhD; Joan Cook, PhD

Arch Dermatol. 1987;123(12):1699-1701.


Abstract

• Deficiency in zinc, an essential trace element, is a frequent human dietary problem in the United States and is also associated with such disease states as alcoholism, renal disease, burns, gastrointestinal tract disorders, and acrodermatitis enteropathica. Skin lesions and poor wound healing are observed in severe forms of the deficiency. However, modest deficits in zinc cause lymphopenia and reduced immune capacity among affected humans. With the mouse used as a model because it has an immune system analogues to that of humans, the effects of zinc deficiency on immune function have been well characterized. A suboptimal intake of zinc causes marked atrophy of the thymus, a 50% reduction in leukocytes, a rise in corticosterone levels, and a 40% to 70% reduction in antibody-mediated, cell-mediated, and delayed-type hypersensitivity responses.

(Arch Dermatol 1987;123:1699-1701)



Author Affiliations

From the Department of Biochemistry, Michigan State University, East Lansing.


Footnotes

Accepted for publication July 29, 1987.

Read before the 36th Annual Symposium on the Biology of Skin ("Molecular Basis of Nutritional Dermatoses"), Salishan Lodge, Gleneden Beach, Ore, Oct 21, 1986.

Reprint requests to Department of Biochemistry, Michigan State University, East Lansing, MI 48823 (Dr Fraker).



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