PD-1+ Tcf1+ CD8+ T cells from established chronic infection can form memory while retaining a stableimprint of persistent antigen exposure.

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7 septembre 2021

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info:eu-repo/semantics/altIdentifier/doi/10.1016/j.celrep.2021.109672

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/34496259

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info:eu-repo/semantics/altIdentifier/eissn/2211-1247

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_2783DEBAC7833

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info:eu-repo/semantics/openAccess , CC BY-NC-ND 4.0 , https://creativecommons.org/licenses/by-nc-nd/4.0/



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Infectious diseases

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M. Charmoy et al., « PD-1+ Tcf1+ CD8+ T cells from established chronic infection can form memory while retaining a stableimprint of persistent antigen exposure. », Serveur académique Lausannois, ID : 10.1016/j.celrep.2021.109672


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Virus-specific PD1 + Tcf1 + memory-like CD8 + T cells (T ML s) maintain the CD8 + T cell response during chronic viral infection. However, the fate of these cells following cessation of persistent antigen exposure has been unclear. Here, we find that T ML s persist upon transfer into antigen-free hosts and form memory following recall stimulation. Phenotypic, functional, and transcriptome analyses show that T ML -derived memory cells resemble those arising in response to acute, resolved infection, but they retain features of chronically stimulated cells, including elevated PD-1 and Tox and reduced cytokine expression. This chronic infection imprint is largely accounted for by constitutive Tox expression. Virus-specific Tcf1 + CD8 + T cells that persist after clearance of systemic infection also display a chronic infection imprint. Notwithstanding, renewed virus exposure induces a recall response, which controls virus infection in part. Thus, cessation of chronic antigen exposure yields a memory CD8 + T cell compartment that reflects prior stimulation.

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