Document Detail


Sustained LFA-1 cluster formation in the immune synapse requires the combined activities of L-plastin and calmodulin.
MedLine Citation:
PMID:  20683899     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Formation of immune synapses (IS) between T cells and APC requires multiple rearrangements in the actin cytoskeleton and selective receptor accumulation in supramolecular activation clusters (SMAC). The inner cluster (central SMAC) contains the TCR/CD3 complex. The outer cluster (peripheral SMAC) contains the integrin LFA-1 and Talin. Molecular mechanisms selectively stabilizing receptors in the IS remained largely unknown. Here, we demonstrate that sustained LFA-1 clustering in the IS is a consequence of the combined activities of the actin-bundling protein L-plastin (LPL) and calmodulin. Thus, upon antigen-recognition of T cells, LPL accumulated predominantly in the peripheral SMAC. siRNA-mediated knock-down of LPL led to a failure of LFA-1 and Talin redistribution - however, not TCR/CD3 relocalization - into the IS. As a result of this LPL knock-down, the T-cell/APC interface became smaller over time and T-cell proliferation was inhibited. Importantly, binding of calmodulin to LPL was required for the maintenance of LPL in the IS and consequently inhibition of calmodulin also prevented stable accumulation of LFA-1 and Talin, but not CD3, in the IS.
Authors:
Guido H Wabnitz; Philipp Lohneis; Henning Kirchgessner; Beate Jahraus; Susan Gottwald; Mathias Konstandin; Martin Klemke; Yvonne Samstag
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of immunology     Volume:  40     ISSN:  1521-4141     ISO Abbreviation:  Eur. J. Immunol.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-02     Completed Date:  2010-11-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  1273201     Medline TA:  Eur J Immunol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  2437-49     Citation Subset:  IM    
Affiliation:
Institute for Immunology, Ruprecht-Karls-University, Heidelberg, Germany. guido.wabnitz@immu.uni-heidelberg.de
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MeSH Terms
Descriptor/Qualifier:
Actins / genetics,  immunology,  metabolism*
Antigen-Presenting Cells / immunology,  metabolism,  pathology
Binding Sites / genetics
Calmodulin / metabolism*
Cell Line, Tumor
Cell Proliferation
Cloning, Molecular
Enterotoxins / metabolism
Humans
Immunological Synapses / genetics,  immunology,  metabolism*
Lymphocyte Function-Associated Antigen-1 / immunology,  metabolism
Membrane Glycoproteins / genetics,  immunology,  metabolism*
Microfilament Proteins / genetics,  immunology,  metabolism*
Microscopy, Confocal
Mutagenesis, Site-Directed
Protein Binding / genetics
Protein Transport / drug effects,  genetics
RNA, Small Interfering / genetics
Sequence Deletion / genetics
Sulfonamides / pharmacology
T-Lymphocytes / drug effects,  immunology,  metabolism*,  pathology
Chemical
Reg. No./Substance:
0/Actins; 0/Calmodulin; 0/Enterotoxins; 0/Lymphocyte Function-Associated Antigen-1; 0/Membrane Glycoproteins; 0/Microfilament Proteins; 0/RNA, Small Interfering; 0/Sulfonamides; 0/plastin; 39424-53-8/enterotoxin B, staphylococcal; 65595-90-6/W 7

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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