[HTML][HTML] PKCθ regulates T cell motility via ezrin-radixin-moesin localization to the uropod

JL Cannon, F Asperti-Boursin, KA Letendre, IK Brown… - PLoS …, 2013 - journals.plos.org
JL Cannon, F Asperti-Boursin, KA Letendre, IK Brown, KE Korzekwa, KM Blaine…
PLoS One, 2013journals.plos.org
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 …
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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