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The Journal of Immunology, 2002, 169: 5021-5027.
Copyright © 2002 by The American Association of Immunologists

Age-Dependent Defects in TCR-Triggered Cytoskeletal Rearrangement in CD4+ T Cells1

Gonzalo G. Garcia* and Richard A. Miller2,*,{dagger},{ddagger}

* Department of Pathology, School of Medicine, and {dagger} Institute of Gerontology, University of Michigan, Ann Arbor, MI 48109; and {ddagger} Ann Arbor Department of Veterans’ Affairs Medical Center, Ann Arbor, MI 48109

Previous research has shown that many of the CD4 T cells from older mice do not form functional immune synapses after conjugation with peptide-pulsed APC. We now show that the defect lies at a very early stage in the cytoskeletal reorganization that precedes movement of protein kinases and their substrates to the TCR/APC interface. Antagonist peptides presented to T cells from young mice induce migration of talin (but not paxillin, vinculin, or F-actin) to the APC contact zone, but CD4 T cells from older donors typically fail to show the talin polarization response. A spreading assay in which contact with anti-CD3-coated slides induces CD4 T cells to assume a conical shape and develop lammelopodia also shows a decline with age in the proportion of T cells that can initiate cytoskeletal changes in response to this simplified stimulus. Finally, the transition from detergent-soluble to cytoskeletal forms of the p16, p21, and p23 isoforms of CD3{zeta} in response to CD3/CD4/CD28 cross-linking is much stronger in young than in old T cells. Thus, defects in cytoskeletal reorganization triggered by initial contact between TCR and peptide-bearing APC precede, and presumably contribute to, defective activation of protein kinase-mediated signals in the first few minutes of the activation cascade in T cells from aged mice.




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