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Am J Physiol Cell Physiol 284: C415-C421, 2003. First published October 16, 2002; doi:10.1152/ajpcell.00365.2002
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Vol. 284, Issue 2, C415-C421, February 2003

Interleukin-2 receptor-gamma -dependent endocytosis depends on biotin in Jurkat cells

Rocio Rodriguez-Melendez1, Gabriela Camporeale1, Jacob B. Griffin1, and Janos Zempleni1,2

Departments of 1 Nutritional Science and Dietetics and 2 Biochemistry, University of Nebraska at Lincoln, Lincoln, Nebraska 68583

Biotin has been credited with having beneficial effects on immune function despite observations that biotin supplementation causes decreased secretion of interleukin-2. Here this paradox was addressed by determining whether receptor-dependent internalization of interleukin-2 by immune cells depends on biotin. Theoretically, this would be consistent with both decreased net secretion of interleukin-2 by biotin-supplemented cells (causing increased endocytosis) and beneficial effects of biotin on immune function (causing increased receptor signaling). Jurkat cells were cultured in biotin-defined media (25, 250, or 10,000 pM). Secretion of interleukin-2 correlated negatively with biotin supply, but transcriptional activity of the interleukin-2 gene correlated positively with biotin supply, suggesting that decreased secretion of interleukin-2 by biotin-supplemented cells was not caused by decreased gene expression. Expression of the interleukin-2 receptor-gamma gene was greater at 10,000 pM than 25 pM biotin, mediating increased endocytosis of interleukin-2 in biotin-supplemented medium. Inhibition of endocytosis by genistein and overexpression of interleukin-2 receptor-gamma abolished the effect of biotin. These findings suggest that endocytosis of interleukin-2 depends on biotin.

cytokines; gene expression; propionyl-CoA carboxylase


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