The alarmin interleukin-33 promotes the expansion and preserves the stemness of Tcf-1+ CD8+ T cells in chronic viral infection.

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11 avril 2023

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info:eu-repo/semantics/altIdentifier/doi/10.1016/j.immuni.2023.01.029

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info:eu-repo/semantics/altIdentifier/pmid/36809763

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info:eu-repo/semantics/altIdentifier/eissn/1097-4180

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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_796365D38E1A0

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



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Infectious diseases

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A.F. Marx et al., « The alarmin interleukin-33 promotes the expansion and preserves the stemness of Tcf-1+ CD8+ T cells in chronic viral infection. », Serveur académique Lausannois, ID : 10.1016/j.immuni.2023.01.029


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T cell factor 1 (Tcf-1) expressing CD8 + T cells exhibit stem-like self-renewing capacity, rendering them key for immune defense against chronic viral infection and cancer. Yet, the signals that promote the formation and maintenance of these stem-like CD8 + T cells (CD8 + SL) remain poorly defined. Studying CD8 + T cell differentiation in mice with chronic viral infection, we identified the alarmin interleukin-33 (IL-33) as pivotal for the expansion and stem-like functioning of CD8 + SL as well as for virus control. IL-33 receptor (ST2)-deficient CD8 + T cells exhibited biased end differentiation and premature loss of Tcf-1. ST2-deficient CD8 + SL responses were restored by blockade of type I interferon signaling, suggesting that IL-33 balances IFN-I effects to control CD8 + SL formation in chronic infection. IL-33 signals broadly augmented chromatin accessibility in CD8 + SL and determined these cells' re-expansion potential. Our study identifies the IL-33-ST2 axis as an important CD8 + SL-promoting pathway in the context of chronic viral infection.

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