Abstract

Tissue-resident memory T cells (TRM cells) have crucial functions in host defense in mucosal tissues. They provide local adaptive immune surveillance and allow the fast initiation of targeted adaptive immune responses in case of antigen re-exposure. Recently, an aberrant activation in the case of immunologically mediated diseases has been increasingly acknowledged. As the organ with the largest interface to the environment, the gastrointestinal tract faces billions of antigens every day. Tightly balanced processes are necessary to ensure tolerance towards non-hazardous antigens, but to set up a powerful immune response against potentially dangerous ones. In this complex nexus of immune cells and their mediators, TRM cells play a central role and have been shown to promote both physiological and pathological events. In this review, we will summarize the current knowledge on the homeostatic functions of TRM cells and delineate their implication in infection control in the gut. Moreover, we will outline their commitment in immune dysregulation in gastrointestinal chronic inflammatory conditions and shed light on TRM cells as current and potential future therapeutic targets.

Highlights

  • Coordinated processes of the immune system require a tightly regulated interplay of various immune cell types and mediators

  • TRM cells persist at epithelial surfaces including the gastrointestinal tract (GIT), skin, and lung as well as in non-barrier tissues such as the brain and the joints [3, 5,6,7,8,9]

  • CD103 pairs with the b7 integrin chain and the heterodimer binds to E-cadherin, which is expressed on epithelial cells [21]. This interaction constitutes an independent mechanism promoting mucosal retention. It was already shown in humans and in mice that the expression of CD103 is more predominant in CD8+ TRM cells than in CD4+

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Summary

Introduction

Coordinated processes of the immune system require a tightly regulated interplay of various immune cell types and mediators. Kumar and colleagues described a transcriptional and phenotypic signature that defines both CD8+ and CD4+ TRM cells in humans and that is conserved across individuals and in mucosal and lymphoid tissues [12]. It was already shown in humans and in mice that the expression of CD103 is more predominant in CD8+ TRM cells than in CD4+ Hobit and Blimp-1 are known to synergistically control the expression of TRM cell-regulated genes like CD69, KLF2, and S1PR1 [27,28,29].

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