HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Garcia, G. G. Articles by Miller, R. A. Search for Related Content PubMed PubMed Citation Articles by Garcia, G. G. Articles by Miller, R. A.

Age-Related Defects in Moesin/Ezrin Cytoskeletal Signals in Mouse CD4 T Cells¹

Gonzalo G. Garcia^*, Amir A. Sadighi Akha^* and Richard A. Miller^2,*,,

^* Department of Pathology, University of Michigan School of Medicine, University of Michigan Geriatrics Center, and Ann Arbor Department of Veterans Affairs Medical Center, Ann Arbor, MI 48109

Cytoskeletal proteins of the ezrin-radixin-moesin (ERM) family contribute to T cell activation in response to Ag, and also to T cell polarization in response to connective tissue matrix proteins and chemokine gradients. Previous work has shown that T cells from aged mice are defective in their ability to develop molecular linkages between surface macromolecules and the underlying cytoskeletal framework, both for proteins that move to the synapse and those that are excluded from the site of T cell-APC interaction. T cells from aged mice also show defective cytoskeletal rearrangements and lamellipodia formation when placed in contact with slides coated with Abs to the TCR/CD3 complex. In this study, we show that old CD4 T cells differ from young CD4 T cells in several aspects of ERM biochemistry, including ERM phosphorylation and ERM associations with CD44, CD43, and EBP50. In addition, CD4 T cells from aged mice show defects in the Rho GTPase activities known to control ERM function.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grants AG19619 and AG024824 from the National Institutes of Health.

² Address correspondence and reprint requests to Dr. Richard A. Miller, Room 3001 Biomedical Sciences Research Building, Box 2200, University of Michigan Medical School, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200. E-mail address: millerr{at}umich.edu

³ Abbreviations used in this paper: ERM, ezrin-radixin-moesin; EBP, ezrin binding protein; OSGE, O-sialoglycoprotein endopeptidase; LAT, linker for activation of T cell; MDR, multidrug-resistant.