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TCR Affinity Promotes CD8⁺ T Cell Expansion by Regulating Survival¹

Immunology Division, Walter and Eliza Hall Institute, Parkville, Victoria, Australia

Ligation with high affinity ligands are known to induce T lymphocytes to become fully activated effector cells while ligation with low affinity ligands (or partial agonists) may result in a delayed or incomplete response. We have examined the quantitative features of CD8⁺ T cell proliferation induced by peptides of different TCR affinities at a range of concentrations in the mouse OT-I model. Both the frequency of cells responding and the average time taken for cells to reach their first division are affected by peptide concentration and affinity. Consecutive division times, however, remained largely unaffected by these variables. Importantly, we identified affinity to be the sole regulator of cell death in subsequent division. These results suggest a mechanism whereby TCR affinity detection can modulate the subsequent rate of T cell growth and ensure the dominance of higher affinity clones over time.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Health and Medical Research Council (to P.D.H.), the Deutsche Forschungsgemeinschaft, and the Human Frontiers Science Program (to M.H.).

² Address correspondence and reprint requests to Dr. Mirja Hommel, The Walter and Eliza Hall Institute, 1G Royal Parade, Parkville, Victoria 3050, Australia. E-mail address: hommel{at}wehi.edu.au

³ Abbreviations used in this paper: hIL-2, human IL-2; N, OVA-derived peptide SIINFEKL.

⁴ The online version of this article contains supplementary material.