Blood-thirsty: S1PR5 and TRM

Hallisey, Victoria; Schwab, Susan R.

doi:10.1084/jem.20211971

Cited by 4 publications

(6 citation statements)

References 14 publications

(20 reference statements)

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“…Interestingly, S1PR5 does not interact with CD69. 21 In contrast to S1PR1, which is directly controlled by KLF2, S1PR5 is regulated via T-bet and Zeb2, 20 demonstrating how tissue residency is the result of multiple coordinated adaptation processes by T cells. Downregulation of S1P receptors is accompanied by the downregulation of the T-box transcription factors T-bet and Eomes, which subsequently renders T RM cells responsive to TGFβ.…”

Section: Common Adaptations Of Memory T Cells To Tissue Residencymentioning

confidence: 99%

“…CD69 is a c‐type lectin protein that can form a complex with S1PR1 and inhibit binding of S1P to S1PR1, thus hindering egress from tissues of T RM cells 3 . A recent study showed that downregulation of S1PR5, another receptor for S1P, is essential for T RM formation in the skin, 20,21 where S1PR5 deficiency leads to enhanced T RM formation. Interestingly, S1PR5 does not interact with CD69 21 .…”

Section: Introductionmentioning

confidence: 99%

“…A recent study showed that downregulation of S1PR5, another receptor for S1P, is essential for T RM formation in the skin, 20,21 where S1PR5 deficiency leads to enhanced T RM formation. Interestingly, S1PR5 does not interact with CD69 21 . In contrast to S1PR1, which is directly controlled by KLF2, S1PR5 is regulated via T‐bet and Zeb2, 20 demonstrating how tissue residency is the result of multiple coordinated adaptation processes by T cells.…”

Section: Introductionmentioning

confidence: 99%

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Insights into phenotypic and functional CD8⁺ T_RM heterogeneity

Heeg

Goldrath

2023

Immunological Reviews

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Summary Cytotoxic CD8+ T cells recognize and eliminate infected or cancerous cells. A subset of CD8+ memory T cells called tissue‐resident memory T cells (TRM) resides in peripheral tissues, monitors the periphery for pathogen invasion, and offers a rapid and potent first line of defense at potential sites of re‐infection. TRM cells are found in almost all tissues and are transcriptionally and epigenetically distinct from circulating memory populations, which shows their ability to acclimate to the tissue environment to allow for long‐term survival. Recent work and the broader availability of single‐cell profiling have highlighted TRM heterogeneity among different tissues, as well as identified specialized subsets within individual tissues, that are time and infection dependent. TRM cell phenotypic and transcriptional heterogeneity has implications for understanding TRM function and longevity. This review aims to summarize and discuss the latest findings on CD8+ TRM heterogeneity using single‐cell molecular profiling and explore the potential implications for immune protection and the design of immune therapies.

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Section: Common Adaptations Of Memory T Cells To Tissue Residencymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Insights into phenotypic and functional CD8⁺ T_RM heterogeneity

Heeg

Goldrath

2023

Immunological Reviews

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“…50 One possible explanation for the effect on entry is that S1PR5 seems less sensitive to ligand-induced internalization than S1PR1. 48,92 Thus, T cells in blood that express S1PR5 may experience a continued pull toward circulatory S1P that counters signals promoting entry into tissues. By contrast, T cells fully lose surface S1PR1 in blood due to ligand-induced internalization; blocking S1PR1 internalization by deletion of the kinase Grk2 delays T cell entry into lymph nodes, and entry of GRK2-KO T cells into lymph nodes from blood is restored with loss of blood S1P.…”

Section: Role Of S1p Signaling In T Cell Exit From Nonlymphoid Tissuesmentioning

confidence: 99%

“…Interestingly, forced expression of S1pr5 not only promoted effector T cell exit from tissues but also limited effector T cell entry into skin 50 . One possible explanation for the effect on entry is that S1PR5 seems less sensitive to ligand‐induced internalization than S1PR1 48,92 . Thus, T cells in blood that express S1PR5 may experience a continued pull toward circulatory S1P that counters signals promoting entry into tissues.…”

Section: S1p Signaling In Exit From Non‐lymphoid Organs During An Imm...mentioning

confidence: 99%

Get me out of here: Sphingosine 1‐phosphate signaling and T cell exit from tissues during an immune response

Hallisey

Schwab

2023

Immunological Reviews

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SummaryDuring an immune response, the duration of T cell residence in lymphoid and non‐lymphoid tissues likely affects T cell activation, differentiation, and memory development. The factors that govern T cell transit through inflamed tissues remain incompletely understood, but one important determinant of T cell exit from tissues is sphingosine 1‐phosphate (S1P) signaling. In homeostasis, S1P levels are high in blood and lymph compared to lymphoid organs, and lymphocytes follow S1P gradients out of tissues into circulation using varying combinations of five G‐protein coupled S1P receptors. During an immune response, both the shape of S1P gradients and the expression of S1P receptors are dynamically regulated. Here we review what is known, and key questions that remain unanswered, about how S1P signaling is regulated in inflammation and in turn how S1P shapes immune responses.

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Role of sphingosine 1-phosphate (S1P) in sepsis-associated intestinal injury

Sun,

Wang,

Zhu

et al. 2023

Front. Med.

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Sphingosine-1-phosphate (S1P) is a widespread lipid signaling molecule that binds to five sphingosine-1-phosphate receptors (S1PRs) to regulate downstream signaling pathways. Sepsis can cause intestinal injury and intestinal injury can aggravate sepsis. Thus, intestinal injury and sepsis are mutually interdependent. S1P is more abundant in intestinal tissues as compared to other tissues, exerts anti-inflammatory effects, promotes immune cell trafficking, and protects the intestinal barrier. Despite the clinical importance of S1P in inflammation, with a very well-defined mechanism in inflammatory bowel disease, their role in sepsis-induced intestinal injury has been relatively unexplored. In addition to regulating lymphocyte exit, the S1P-S1PR pathway has been implicated in the gut microbiota, intestinal epithelial cells (IECs), and immune cells in the lamina propria. This review mainly elaborates on the physiological role of S1P in sepsis, focusing on intestinal injury. We introduce the generation and metabolism of S1P, emphasize the maintenance of intestinal barrier homeostasis in sepsis, and the protective effect of S1P in the intestine. We also review the link between sepsis-induced intestinal injury and S1P-S1PRs signaling, as well as the underlying mechanisms of action. Finally, we discuss how S1PRs affect intestinal function and become targets for future drug development to improve the translational capacity of preclinical studies to the clinic.

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Blood-thirsty: S1PR5 and TRM

Cited by 4 publications

References 14 publications

Insights into phenotypic and functional CD8⁺ T_RM heterogeneity

Insights into phenotypic and functional CD8⁺ T_RM heterogeneity

Get me out of here: Sphingosine 1‐phosphate signaling and T cell exit from tissues during an immune response

Role of sphingosine 1-phosphate (S1P) in sepsis-associated intestinal injury

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Blood-thirsty: S1PR5 and TRM

Cited by 4 publications

References 14 publications

Insights into phenotypic and functional CD8+ TRM heterogeneity

Insights into phenotypic and functional CD8+ TRM heterogeneity

Get me out of here: Sphingosine 1‐phosphate signaling and T cell exit from tissues during an immune response

Role of sphingosine 1-phosphate (S1P) in sepsis-associated intestinal injury

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Insights into phenotypic and functional CD8⁺ T_RM heterogeneity

Insights into phenotypic and functional CD8⁺ T_RM heterogeneity