The viral context instructs the redundancy of costimulatory pathways in driving CD8+ T cell expansion

Abstract: Signals delivered by costimulatory molecules are implicated in driving T cell expansion. The requirements for these signals, however, vary from dispensable to essential in different infections. We examined the underlying mechanisms of this differential T cell costimulation dependence and found that the viral context determined the dependence on CD28/B7-mediated costimulation for expansion of naive and memory CD8+ T cells, indicating that the requirement for costimulatory signals is not imprinted. Notably, related to the high-level costimulatory molecule expression induced by lymphocytic choriomeningitis virus (LCMV), CD28/B7-mediated costimulation was dispensable for accumulation of LCMV-specific CD8+ T cells because of redundancy with the costimulatory pathways induced by TNF receptor family members (i.e., CD27, OX40, and 4-1BB). Type I IFN signaling in viral-specific CD8+ T cells is slightly redundant with costimulatory signals. These results highlight that pathogen-specific conditions differentially and uniquely dictate the utilization of costimulatory pathways allowing shaping of effector and memory antigen-specific CD8+ T cell responses

Location
Deutsche Nationalbibliothek Frankfurt am Main
Extent
Online-Ressource
Language
Englisch
Notes
eLife. - 4 (2015) , e07486, ISSN: 2050-084X

Event
Veröffentlichung
(where)
Freiburg
(who)
Universität
(when)
2019
Creator
Welten, Suzanne P. M.
Redeker, Anke
Franken, Kees L. M. C
Oduro, Jennifer Dora
Ossendorp, Ferry
Cicin-Sain, Luka
Melief, Cornelis J. M
Aichele, Peter
Arens, Ramon
Contributor

DOI
10.7554/elife.07486
URN
urn:nbn:de:bsz:25-freidok-1274415
Rights
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Last update
25.03.2025, 1:46 PM CET

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Associated

Time of origin

  • 2019

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