title: The sialyltransferase ST3Gal-I is not required for regulation of CD8-class I MHC binding during T cell development.
abstract: The CD8 coreceptor plays a crucial role in thymocyte and T cell sensitivity by binding to class I MHC and recruiting downstream signaling molecules to the TCR. Previous studies reported considerable changes in TCR-independent CD8/class I MHC binding (i.e., CD8 noncognate interactions) during T cell development, changes that correlated with altered glycosylation of surface molecules. In particular, expression of the sialyltransferase ST3Gal-I has been proposed as a critical factor regulating the attenuation of CD8 avidity during the double-positive to CD8 single-positive progression. This hypothesis is strengthened by the fact that ST3Gal-I(-/-) animals show a profound disregulation of CD8 T cell homeostasis. In contrast to this model, however, we report in this study that ST3Gal-I deficiency had no detectable impact on CD8 noncognate binding to multimeric peptide/MHC class I ligands at any stage of thymocyte development. We also found that the susceptibility to CD8-induced cell death is not markedly influenced by ST3Gal-I deficiency. Thus, the profound effects of ST3Gal-I on CD8 T cell survival evidently do not involve a role for this enzyme in controlling CD8-class I binding.
authors.affiliation: University of Minnesota, Center for Immunology, Department of Laboratory Medicine and Pathology, Minneapolis, 55455, USA.
authors.forename: Charlly
authors.initials: C
authors.lastname: Kao
authors.forename: Michelle M
authors.initials: MM
authors.lastname: Sandau
authors.forename: Mark A
authors.initials: MA
authors.lastname: Daniels
authors.forename: Stephen C
authors.initials: SC
authors.lastname: Jameson
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000276:immunology; D016827:CD8 Antigens / Q000096:biosynthesis / Q000276:immunology / Q000378:metabolism*; D018414:CD8-Positive T-Lymphocytes / Q000166:cytology / Q000201:enzymology / Q000276:immunology; D002454:Cell Differentiation / Q000235:genetics / Q000276:immunology*; D015395:Histocompatibility Antigens Class I / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008822:Mice, Transgenic; D011485:Protein Binding / Q000235:genetics / Q000276:immunology; D011948:Receptors, Antigen, T-Cell / Q000378:metabolism*; D012794:Sialic Acids / Q000378:metabolism; D012799:Sialyltransferases / Q000172:deficiency / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D016176:T-Lymphocyte Subsets / Q000166:cytology* / Q000201:enzymology / Q000276:immunology; D013950:Thymus Gland / Q000166:cytology* / Q000201:enzymology / Q000276:immunology; D000094663:beta-Galactoside alpha-2,3-Sialyltransferase
chemical_list: D016827:CD8 Antigens; C067361:CD8 receptor; D015395:Histocompatibility Antigens Class I; D011948:Receptors, Antigen, T-Cell; D012794:Sialic Acids; D012799:Sialyltransferases; D000094663:beta-Galactoside alpha-2,3-Sialyltransferase