2014
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.4049/jimmunol.1302289
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/24273000
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/1550-6606
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_7FE9BEB468C77
info:eu-repo/semantics/openAccess , Copying allowed only for non-profit organizations , https://serval.unil.ch/disclaimer
D. Zehn et al., « Inflammation and TCR Signal Strength Determine the Breadth of the T Cell Response in a Bim-Dependent Manner. », Serveur académique Lausannois, ID : 10.4049/jimmunol.1302289
Generating a diverse T cell memory population through vaccination is a promising strategy to overcome pathogen epitope variability and tolerance to tumor Ags. The effector and memory pool becomes broad in TCR diversity by recruiting high- and low-affinity T cells. We wanted to determine which factors dictate whether a memory T cell pool has a broad versus focused repertoire. We find that inflammation increases the magnitude of low- and high-affinity T cell responses equally well, arguing against a synergistic effect of TCR and inflammatory signals on T cell expansion. We dissect the differential effects of TCR signal strength and inflammation and demonstrate that they control effector T cell survival in a bim-dependent manner. Importantly, bim-dependent cell death is overcome with a high Ag dose in the context of an inflammatory environment. Our data define the framework for the generation of a broad T cell memory pool to inform future vaccine design.