BMB Rep. 2015; 48(7): 369-370  
TAGLN2-mediated actin stabilization at the immunological synapse: implication for cytotoxic T cell control of target cells
Bo-Ra Na & Chang-Duk Jun*
School of Life Sciences, Immune Synapse Research Center and Cell Dynamics Research Center, GIST, Gwangju 500-712, Korea
Correspondence to: E-mail: cdjun@gist.ac.kr
Received: June 29, 2015; Published online: July 31, 2015.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

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.
Keywords: TAGLN2, Actin stabilization, Immunological synapse, T cell activation


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