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TAGLN2-mediated actin stabilization at the immunological synapse: implication for cytotoxic T cell control of target cells
TAGLN2-mediated actin stabilization at the immunological synapse: implication for cytotoxic T cell control of target cells
BMB Reports. 2015. Jul, 48(7): 369-370
Copyright © 2015, Korean Society for Biochemistry and Molecular Biology
This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
  • Received : June 29, 2015
  • Published : July 31, 2015
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Bo-Ra Na
Chang-Duk Jun
cdjun@gist.ac.kr

Abstract
Actin dynamics is critical for the formation and sustainment of the immunological synapse (IS) during T cell interaction with antigen-presenting cells (APC). Thus, many actin regulating proteins are involved in spatial and temporal actin remodeling at the IS. However, little is known whether or how actin stabilizing protein controls IS and the consequent T cell functions. TAGLN2 − an actin-binding protein predominantly expressed in T cells − displays a novel function to stabilize cortical F-actin, thereby augmenting F-actin contents at the IS, and acquiring leukocyte function-associated antigen-1 activation following T cell activation. TAGLN2 also competes with cofilin to protect F-actin in vitro and in vivo . During cytotoxic T cell interaction with cancer cells, the expression level of TAGLN2 at the IS correlates with the T cell adhesion to target cancer cells and production of lytic granules such as granzyme B and perforin, thus expressing cytotoxic T cell function. These findings identify a novel function for TAGLN2 as an actin stabilizing protein that is essential for stable immunological synapse formation, thereby regulating T cell immunity. [BMB Reports 2015; 48(7): 369-370]
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Acknowledgements
This work was supported by the Basic Science Research Program (2012R1A2A1A03002115), Basic Science Research Program through the National Research Foundation (NRF) of Korea funded by the Ministry of Education (2013R1A6A3A04 064259), and Cell Dynamics Research Center Program (2007-0056244) through the NRF grants funded by the Ministry of Science, ICT and Future Planning, Korea. This work was also partially supported by the Bio-Imaging Research Center at GIST.
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