Published November 8, 2013 | Version v1
Journal article Open

PKCθ Regulates T Cell Motility via Ezrin-Radixin-Moesin Localization to the Uropod

Description

Cell motility is a fundamental process crucial for function in many cell types, including T cells. T cell motility is critical for T cell-mediated immune responses, including initiation, activation, and effector function. While many extracellular receptors and cytoskeletal regulators have been shown to control T cell migration, relatively few signaling mediators have been identified that can modulate T cell motility. In this study, we find a previously unknown role for PKCθ in regulating T cell migration to lymph nodes. PKCθ localizes to the migrating T cell uropod and regulates localization of the MTOC, CD43 and ERM proteins to the uropod. Furthermore, PKCθ-deficient T cells are less responsive to chemokine induced migration and are defective in migration to lymph nodes. Our results reveal a novel role for PKCθ in regulating T cell migration and demonstrate that PKCθ signals downstream of CCR7 to regulate protein localization and uropod formation.

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Additional details

Identifiers

DOI
10.1371/journal.pone.0078940
Other
oai:uchicago.tind.io:10556

Funding

American Heart Association
Scientist Development Grant
American Cancer Society
Internal Research Grant
University of New Mexico
National Institutes of Health
5R01AI097202
Irvington Institute
Fellowship Program of the Cancer Research Institute
U.S. National Science Foundation
1038682
Defense Advanced Research Projects Agency
1070-113237

UChicago Information

Division(s)
Biological Sciences Division
Department(s)
Medicine