Interleukin-2 receptor-γ-dependent endocytosis depends on biotin in jurkat cells

Rocio Rodriguez-Melendez, Gabriela Camporeale, Jacob B. Griffin, Janos Zempleni

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

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-γ 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-γ abolished the effect of biotin. These findings suggest that endocytosis of interleukin-2 depends on biotin.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Cell Physiology
Volume284
Issue number2 53-2
StatePublished - Feb 1 2003

Fingerprint

Jurkat Cells
Interleukin-2 Receptors
Biotin
Endocytosis
Interleukin-2
Genes
Genistein
Gene expression

Keywords

  • Cytokines
  • Gene expression
  • Propionyl-CoA carboxylase

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

Cite this

Interleukin-2 receptor-γ-dependent endocytosis depends on biotin in jurkat cells. / Rodriguez-Melendez, Rocio; Camporeale, Gabriela; Griffin, Jacob B.; Zempleni, Janos.

In: American Journal of Physiology - Cell Physiology, Vol. 284, No. 2 53-2, 01.02.2003.

Research output: Contribution to journalArticle

Rodriguez-Melendez, Rocio ; Camporeale, Gabriela ; Griffin, Jacob B. ; Zempleni, Janos. / Interleukin-2 receptor-γ-dependent endocytosis depends on biotin in jurkat cells. In: American Journal of Physiology - Cell Physiology. 2003 ; Vol. 284, No. 2 53-2.
@article{41e4a308bb4144ba84812dd935fd97bb,
title = "Interleukin-2 receptor-γ-dependent endocytosis depends on biotin in jurkat cells",
abstract = "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-γ 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-γ abolished the effect of biotin. These findings suggest that endocytosis of interleukin-2 depends on biotin.",
keywords = "Cytokines, Gene expression, Propionyl-CoA carboxylase",
author = "Rocio Rodriguez-Melendez and Gabriela Camporeale and Griffin, {Jacob B.} and Janos Zempleni",
year = "2003",
month = "2",
day = "1",
language = "English (US)",
volume = "284",
journal = "American Journal of Physiology - Renal Physiology",
issn = "0363-6127",
publisher = "American Physiological Society",
number = "2 53-2",

}

TY - JOUR

T1 - Interleukin-2 receptor-γ-dependent endocytosis depends on biotin in jurkat cells

AU - Rodriguez-Melendez, Rocio

AU - Camporeale, Gabriela

AU - Griffin, Jacob B.

AU - Zempleni, Janos

PY - 2003/2/1

Y1 - 2003/2/1

N2 - 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-γ 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-γ abolished the effect of biotin. These findings suggest that endocytosis of interleukin-2 depends on biotin.

AB - 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-γ 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-γ abolished the effect of biotin. These findings suggest that endocytosis of interleukin-2 depends on biotin.

KW - Cytokines

KW - Gene expression

KW - Propionyl-CoA carboxylase

UR - http://www.scopus.com/inward/record.url?scp=0037302162&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037302162&partnerID=8YFLogxK

M3 - Article

VL - 284

JO - American Journal of Physiology - Renal Physiology

JF - American Journal of Physiology - Renal Physiology

SN - 0363-6127

IS - 2 53-2

ER -