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Articles in PresS, published online ahead of print October 16, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00365.2002
Submitted on August 12, 2002
Accepted on December 31, 1969
-dependent Endocytosis Depends on Biotin in Jurkat Cells
1 Nutritional Science and Dietetics, University of Nebraska-Lincoln, Lincoln, NE, USA
2 Nutritional Science and Dietetics, University of Nebraska-Lincoln, Lincoln, NE, USA; Biochemistry, University of Nebraska-Lincoln, Lincoln, NE, USA
* To whom correspondence should be addressed. E-mail: jzempleni2{at}unl.edu.
Biotin has been credited for having beneficial effects on immune function, despite of 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 
gene was greater at 10,000 pM compared to 25 pM biotin, mediating increased endocytosis of interleukin-2 in biotin-supplemented medium. Inhibition of endocytosis by genistein and overexpression of interleukin-2 receptor abolished the effect of biotin. These findings suggest that endocytosis of interleukin-2 depends on biotin.
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