Murine CD8 T‐cell functional avidity is stable in vivo but not in vitro: Independence from homologous prime/boost time interval and antigen density
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Gilfillan_et_al-2019-European_Journal_of_Immunology.pdf
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Published version
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601.9 KB
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Author(s)
Gilfillan, Connie B.
Wang, Chensu
Mohsen, Mona O.
Rufer, Nathalie
Hebeisen, Michael
Allard, Mathilde
Verdeil, Grégory
Bachmann, Martin F.
Speiser, Daniel E.
Irvine, Darrell J. (Darrell John), 1973-
Date Issued
November 2019
Journal
European Journal of Immunology
Publisher
Wiley
Citation
Gilfillan, Connie B. et al. "Murine CD8 T‐cell functional avidity is stable in vivo but not in vitro: Independence from homologous prime/boost time interval and antigen density." European Journal of Immunology 50, 4 (April 2020): 505-514 © 2019 The Authors
Version
Final published version
Abstract
It is known that for achieving high affinity antibody responses, vaccines must be optimized for antigen dose/density, and the prime/boost interval should be at least 4 weeks. Similar knowledge is lacking for generating high avidity T-cell responses. The functional avidity (FA) of T cells, describing responsiveness to peptide, is associated with the quality of effector function and the protective capacity in vivo. Despite its importance, the FA is rarely determined in T-cell vaccination studies. We addressed the question whether different time intervals for short-term homologous vaccinations impact the FA of CD8 T-cell responses. Four-week instead of 2-week intervals between priming and boosting with potent subunit vaccines in C57BL/6 mice did not improve FA. Equally, similar FA was observed after vaccination with virus-like particles displaying low versus high antigen densities. Interestingly, FA was stable in vivo but not in vitro, depending on the antigen dose and the time interval since T-cell activation, as observed in murine monoclonal T cells. Our findings suggest dynamic in vivo modulation for equal FA. We conclude that low antigen density vaccines or a minimal 4-week prime/boost interval are not crucial for the T-cell's FA, in contrast to antibody responses.
MIT Department
Koch Institute for Integrative Cancer Research at MIT
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Creative Commons Attribution 4.0 International license
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DOI of Published Version
https://doi.org/10.1002/eji.201948355
