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. 2021 Nov 6;15(3):389–397. doi: 10.1038/s41385-021-00467-7

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — TRMs are found in mucosal tissues following different infections. They are known to express variable levels of the tissue retention markers CD69 and CD103. Following IAV infection CD8 + TRMs infiltrate the lung epithelium and induce cell death in the targeted cells through perforin/granzyme delivery as well asl FasL/Fas pathways and produce IFNγ, TNF, IL-2, and other cytokines and chemokines to enhance inflammation and immune activation in the infected lung tissue. HIV-specific CD8 + TRMs express CD69 and intermediate levels of CD103 in the gut mucosal epithelium, where they secrete granzyme A, IFNγ and TNF against HIV-infected cells. In the tonsil, EBV-specific CD8 + TRMs localize at the lymphoepithelial barrier, where most EBV + B cells are found. Tonsillar EBV-specific CD8 + TRMs are polyfunctional and produce IFN-γ among other cytokines. After intravaginal infections HSV-specific CD8 + TRMs are established in the lower FRT, where they persist in the dermo-epidermal junction and rely on perforin/granzyme and cytokine secretion (mostly IFNγ, but also TNF and RANTES expression) for clearance of infected cells.