PKCθ Regulates T Cell Motility via Ezrin-Radixin-Moesin Localization to the Uropod
Creators
- 1. University of New Mexico
- 2. University of Chicago
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.
Files
journal.pone.0078940.pdf
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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