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International Immunology Advance Access originally published online on November 1, 2005
International Immunology 2005 17(12):1607-1617; doi:10.1093/intimm/dxh340
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© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Loss of CD8 and TCR binding to Class I MHC ligands following T cell activation

Charlly Kao, Mark A. Daniels1 and Stephen C. Jameson

Department of Laboratory Medicine and Pathology, Center for Immunology, University of Minnesota, MMC 334, 420 Delaware Street SE, Minneapolis, MN 55455, USA
1 Present address: Department of Transplantation Immunology and Nephrology, University Hospital Basel, CH 4031 Basel, Switzerland

Correspondence to: S. C. Jameson; E-mail: james024{at}umn.edu

The capacity of T cells to bind peptide/MHC ligands changes with T cell development and differentiation. Here we study changes in peptide/MHC multimer binding following T cell activation. Surprisingly, T cell activation caused a marked reduction in specific peptide/MHC Class I multimer binding, which was distinct from transient TCR down-regulation, and was especially dramatic for engagement with low-affinity peptide/MHC ligands. Direct CD8–Class I interactions were also profoundly and rapidly impaired following T cell stimulation, even though surface CD8{alpha} and CD8ß levels were unchanged after activation, suggesting that decreased CD8 co-receptor binding contributes to this effect. Finally, we show that enzymatic desialylation restores much of the multimer binding on activated T cells, suggesting that altered glycosylation may inhibit TCR/CD8 binding to peptide/MHC ligands. These radical changes in activated T cells' ability to perceive peptide/MHC ligands may contribute to selective outgrowth of clones with high affinity for the stimulatory ligand.

Keywords: activation, CTL, tetramer

Transmitting editor: H. Ploegh


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