T-cell Egression
T-cell Egression - Related Videos
14:56
A Genetic Screen to Isolate Toxoplasma gondii Host-cell Egress Mutants
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Cited by 18 •
2012
Forward genetics is a powerful method to unravel the molecular level of how Toxoplasma egresses from its host cell. Protocols are provided to chemically mutagenize parasites, enrich for mutants with defects in induced egress, and validate the phenotype of cloned mutants.
08:39
Quantifying Leukocyte Egress via Lymphatic Vessels from Murine Skin and Tumors
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Cited by 23 •
2019
Here, we demonstrate the methods for in vivo quantification of leukocyte egress from naïve, inflamed, and malignant murine skin. We perform a head-to-head comparison of two models: transdermal FITC application and in situ photoconversion. Furthermore, we demonstrate the utility of photoconversion for tracking leukocyte egress from cutaneous tumors.
05:14
Studying Interactions between Myeloid Cells and CAR T Cells In Vitro and In Vivo
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2025
Given the limited xenograft models available to study interactions between human CART and myeloid cells, we established in vitro and in vivo models to understand the impacts of human macrophages on CART cells. Findings can potentially be generalized to evaluate macrophage roles in the tumor microenvironment and test macrophage-targeted immunotherapies.
08:04
In Vitro Tumor Cell Rechallenge For Predictive Evaluation of Chimeric Antigen Receptor T Cell Antitumor Function
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Cited by 23 •
2019
Here, we describe an in vitro co-culture method to recursively challenge tumor-targeted T cells, which allows for phenotypic and functional analysis of antitumor T cell activity.
10:04
Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells
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2025
This protocol describes the in vivo reprogramming of mouse cancer cells into type 1 dendritic-like cells within the tumor microenvironment through enforced expression of the transcription factors PU.1, IRF8, and BATF3.
FAQs
S1PR1 provides a directional cue by sensing sphingosine-1-phosphate, a lipid signal, across tissue environments. T cells can use this gradient to orient toward lymphatic exit routes rather than moving without direction. Because receptor-guided positioning links local chemical information to cell movement, changes in this pathway can influence whether activated lymphocytes leave a tissue and re-enter circulation.
Exit requires more than a directional signal: T cells must adjust both their attachment to surrounding structures and their ability to move. Adhesion controls how cells interact with tissue and endothelial surfaces, whereas motility enables them to progress toward an exit. Coordinating these properties allows transit without making cells either immobile or unable to engage the route.
Chemokines add positional information, while endothelial barriers determine whether a T cell can cross from tissue into a vessel. Their combined influence helps regulate where and when transit occurs. Consequently, egression depends on both guidance cues and a permissive cellular boundary, not on S1PR1 sensing alone at the relevant exit site.
Trafficking can be altered by infection, inflammation, cancer, and immunotherapy, so each setting may change how T cells redistribute between tissues and circulation. Evaluating egression in these contexts can reveal whether immune cells remain localized, recirculate, or reach other tissues. That comparison is useful for connecting altered movement with disease or treatment response.
An investigation can follow the linked features that control exit: S1PR1 recognition of lipid gradients, chemokine guidance, changes in adhesion and motility, and interactions with endothelial barriers. Considering these elements together helps distinguish a problem in directional sensing from one involving movement or barrier transit, while also relating cellular behavior to circulation and tissue distribution.
By enabling activated T cells to leave sites of immune activation and recirculate, egression contributes to the resolution of immune responses. It also allows those cells to reach other tissues, extending immune surveillance beyond the site where activation occurred. Studying this movement therefore connects local immune activity with system-wide patterns of lymphocyte distribution.
Altered egression can change which tissues receive activated T cells and how long those cells remain at a site. In cancer or during immunotherapy, that redistribution may help explain differences in immune-cell access and treatment responses. Mapping the relevant exit controls could therefore support strategies aimed at controlling immune-cell distribution rather than viewing trafficking as fixed.