The sialyltransferase ST3Gal-I is not required for regulation of CD8-class I MHC binding during T cell development

Charlly Kao, Michelle M. Sandau, Mark A. Daniels, Stephen C. Jameson

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)7421-7430
Number of pages10
JournalJournal of Immunology
Volume176
Issue number12
DOIs
StatePublished - Jun 15 2006

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