PMID:14635057

Citation	Garcia, GG and Miller, RA (2003) Age-related defects in CD4+ T cell activation reversed by glycoprotein endopeptidase. Eur. J. Immunol. 33:3464-72
Abstract	CD4(+) T cells from old mice show defects in the activation process including deficiency in the formation of immunosynapses with antigen-presenting cells. We show that CD4(+) T cells from old mice express unusually high levels of glycosylated forms of the bulky T cell glycoprotein CD43, particularly on a subset of functionally anergic cells expressing P-glycoprotein. T cells from old donors also show a decline in the association of CD43 with cytoskeletal matrix and in the proportion of T cells that can exclude CD43 from the synapse. O-sialoglycoprotein endopeptidase, which removes the external domain of CD43 and other O-sialoglycoproteins from the aged naive CD4(+) T cells of TCR-transgenic mice, restores early agonist-independent stages and later agonist-dependent stages of synapse formation as well as expression of the activation markers CD69 and CD25 to the levels found in the young mice. These data support a model in which O-glycosylated forms of T cell surface molecules, including CD43, are largely responsible for age-related defects in TCR signaling and function.
Links	PubMed Online version:10.1002/eji.200324310
Keywords	Aging/immunology; Animals; Antigens, CD/analysis; Antigens, CD43; Antigens, Differentiation, T-Lymphocyte/analysis; CD4-Positive T-Lymphocytes/immunology; Cells, Cultured; Cytoskeleton/metabolism; Glycosylation; Lectins, C-Type; Lymphocyte Activation; Metalloendopeptidases/pharmacology; Mice; Protein Isoforms; Protein Transport; Receptors, Interleukin-2/analysis; Sialoglycoproteins/analysis; Sialoglycoproteins/metabolism; Synapses/physiology
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