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. 2021 Oct 4;15(1):64–73. doi: 10.1038/s41385-021-00456-w

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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. 2 — CD8 T cells are activated in secondary lymphoid organs (SLO) where naïve T cells find their cognate antigen delivered by antigen-presenting cells together with cytokines that determine differentiation (panel 1). Activated CD8 T cells (green) are controlled by CD4 T cells (blue) and Treg cells (orange), and undergo clonal expansion, upregulate CD69 and shed CD62L, eventually leaving the SLO as effector T cells after downregulating CD69. Ongoing inflammation will recruit circulating effector T cells, such as via a CXCL10 gradient attracting type 1 effector CD8 T cells (grey) (panel 2). These cells reencounter antigen and re-express CD69. Many expand and differentiate into fully differentiated effector T cells (colour changing indicating increased terminal differentiation). During the early phase, some effector T cells (expressing Tbet and Eomes) will be in close contact with recruited type 1 Treg cells, also expressing CXCR3. The TGFβ expressed by these cells and its activation via Itgβ8 transforms early effector CD8 T cells into Trm cells (purple) via downregulation of Tbet and Eomes and the expression of Hobit, AhR and CD103. After clearance of the pathogen present most effector T cells undergo apoptosis, with few remaining as circulating Tem or Trm that remain at the original site of infection (panel 3). Treg cells may also remain in the tissues, with a substantial type 2 phenotype with expression of ST2, playing a role in tissue repair and homeostasis.