Age-related defects in the cytoskeleton signaling pathways of CD4 T cells.
It has been postulated that the cytoskeleton controls many aspects of T cell function, including activation, proliferation and apoptosis. Recent advances in our understanding of F-actin polymerization and the Ezrin-Radixin-Moesin (ERM) family of cytoskeleton signal proteins have provided new insights into immunological synapse formation during T cell activation. During aging there is a significant decline of T cell function largely attributable to declines in activation of CD4 T cells and defects in the formation of the immunological synapse. Here we discuss recent progress in the understanding of how aging alters F-actin and ERM proteins in mouse CD4 T cells, and the implications of these changes for the T cell activation process.
Garcia
Gonzalo G
GG
Department of Pathology, University of Michigan School of Medicine, Ann Arbor, MI, United States. gonzola@umich.edu
Miller
Richard A
RA
D000375:Aging / Q000502:physiology*; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000502:physiology*; D003598:Cytoskeletal Proteins / Q000502:physiology; D003599:Cytoskeleton / Q000502:physiology*; D006801:Humans; D015398:Signal Transduction / Q000502:physiology*
D003598:Cytoskeletal Proteins