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PLoS One. 2011;6(9):e24667. doi: 10.1371/journal.pone.0024667. Epub 2011 Sep 12.

Involvement of mTOR in CXCL12 mediated T cell signaling and migration.

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  • 1Lymphocyte Cell Biology Unit, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.

Abstract

BACKGROUND:

CXCL12 is a pleiotropic chemokine involved in multiple different processes such as immune regulation, inflammatory responses, and cancer development. CXCL12 is also a potent chemokine involved in chemoattraction of T cells to the site of infection or inflammation. Mammalian target of rapamycin (mTOR) is a serine-threonine kinase that modulates different cellular processes, such as metabolism, nutrient sensing, protein translation, and cell growth. The role of mTOR in CXCL12-mediated resting T cell migration has yet to be elucidated.

METHODOLOGY/PRINCIPAL FINDINGS:

Rapamycin, an inhibitor of mTOR, significantly inhibits CXCL12 mediated migration of both primary human resting T cells and human T cell leukemia cell line CEM. p70(S6K1), an effector molecule of mTOR signaling pathway, was knocked down by shRNA in CEM cells using a lentiviral gene transfer system. Using p70(S6K1) knock down cells, we demonstrate the role of mTOR signaling in T cell migration both in vitro and in vivo.

CONCLUSIONS:

Our data demonstrate a new role for mTOR in CXCL12-induced T cell migration, and enrich the current knowledge regarding the clinical use of rapamycin.

PMID:
21931802
[PubMed - indexed for MEDLINE]
PMCID:
PMC3171460
Free PMC Article
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