T cell receptor signaling strength establishes the chemotactic properties of effector CD8+ T cells that control tissue-residency

Mahmoud Abdelbary, Samuel J. Hobbs, James S. Gibbs, Jonathan W. Yewdell and Jeffrey C. Nolz ()
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Mahmoud Abdelbary: Oregon Health & Science University
Samuel J. Hobbs: Oregon Health & Science University
James S. Gibbs: National Institute of Allergy and Infectious Diseases, National Institutes of Health
Jonathan W. Yewdell: National Institute of Allergy and Infectious Diseases, National Institutes of Health
Jeffrey C. Nolz: Oregon Health & Science University

Nature Communications, 2023, vol. 14, issue 1, 1-14

Abstract: Abstract Tissue-resident memory (TRM) CD8+ T cells are largely derived from recently activated effector T cells, but the mechanisms that control the extent of TRM differentiation within tissue microenvironments remain unresolved. Here, using an IFNγ-YFP reporter system to identify CD8+ T cells executing antigen-dependent effector functions, we define the transcriptional consequences and functional mechanisms controlled by TCR-signaling strength that occur within the skin during viral infection to promote TRM differentiation. TCR-signaling both enhances CXCR6-mediated migration and suppresses migration toward sphingosine-1-phosphate, indicating the programming of a ‘chemotactic switch’ following secondary antigen encounter within non-lymphoid tissues. Blimp1 was identified as the critical target of TCR re-stimulation that is necessary to establish this chemotactic switch and for TRM differentiation to efficiently occur. Collectively, our findings show that access to antigen presentation and strength of TCR-signaling required for Blimp1 expression establishes the chemotactic properties of effector CD8+ T cells to promote residency within non-lymphoid tissues.

Date: 2023
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-39592-1

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DOI: 10.1038/s41467-023-39592-1

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