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Immunodominance of an Antiviral Cytotoxic T Cell Response Is Shaped by the Kinetics of Viral Protein Expression

Hans Christian Probst, Kathrin Tschannen, Awen Gallimore, Marianne Martinic, Michael Basler, Tilman Dumrese, Emma Jones and Maries F. van den Broek
J Immunol November 15, 2003, 171 (10) 5415-5422; DOI: https://doi.org/10.4049/jimmunol.171.10.5415
Hans Christian Probst
*Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland;
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Kathrin Tschannen
*Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland;
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Awen Gallimore
†Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, United Kingdom; and
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Marianne Martinic
*Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland;
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Michael Basler
‡Department of Immunology, University of Constance, Constance, Germany.
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Tilman Dumrese
*Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland;
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Emma Jones
†Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, United Kingdom; and
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Maries F. van den Broek
*Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland;
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Abstract

Lymphocytic choriomeningitis virus (LCMV) infection induces a protective CTL response consisting of gp- and nucleoprotein (NP)-specific CTL. We find that a small load of LCMV led to immunodominance of NP-CTL, whereas a large viral load resulted in dominance of gp-CTL. This is the first study describing that immunodominance is not fixed after infection with a given pathogen, but varies with the viral load instead. We assumed higher Ag sensitivity for NP-CTL, which would explain their preferential priming at low viral load, as well as their overstimulation resulting in selective exhaustion at high viral load. The higher Ag sensitivity of NP-CTL was due to faster kinetics of NP-epitope presentation. Thus, we uncover a novel factor that impinges upon immunodominance and is related to the kinetics of virus protein expression. We propose that CTL against early viral proteins swiftly interfere with virus replication, resulting in efficient protection. If these “early” CTL fail in immediate virus control, they are activated in the face of higher viral load compared with “late” CTL and are therefore prone to be exhausted. Thus, the observed absence of early CTL in persistent infections might not be the cause, but rather the consequence of viral persistence.

  • Received November 12, 2002.
  • Accepted September 3, 2003.
  • Copyright © 2003 by The American Association of Immunologists
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The Journal of Immunology: 171 (10)
The Journal of Immunology
Vol. 171, Issue 10
15 Nov 2003
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Immunodominance of an Antiviral Cytotoxic T Cell Response Is Shaped by the Kinetics of Viral Protein Expression
Hans Christian Probst, Kathrin Tschannen, Awen Gallimore, Marianne Martinic, Michael Basler, Tilman Dumrese, Emma Jones, Maries F. van den Broek
The Journal of Immunology November 15, 2003, 171 (10) 5415-5422; DOI: 10.4049/jimmunol.171.10.5415

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Immunodominance of an Antiviral Cytotoxic T Cell Response Is Shaped by the Kinetics of Viral Protein Expression
Hans Christian Probst, Kathrin Tschannen, Awen Gallimore, Marianne Martinic, Michael Basler, Tilman Dumrese, Emma Jones, Maries F. van den Broek
The Journal of Immunology November 15, 2003, 171 (10) 5415-5422; DOI: 10.4049/jimmunol.171.10.5415
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