T Lymphocyte Adhesion
T Lymphocyte Adhesion - Related Videos
09:14
Static Adhesion Assay for the Study of Integrin Activation in T Lymphocytes
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Cited by 21 •
2014
Static adhesion assay is a powerful tool that can be used to model the interactions between T lymphocytes and other cell types. Interactions are generated by injecting labeled T cells into wells coated with adhesion molecules, while a plate reader is used to quantify the number of adherent cells following serial washes.
07:40
Assay of Adhesion Under Shear Stress for the Study of T Lymphocyte-Adhesion Molecule Interactions
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Cited by 3 •
2016
This flow adhesion assay provides a simple, high impact model of T cell-epithelial cell interactions. A syringe pump is used to generate shear stress, and confocal microscopy captures images for quantification. The goal of these studies is to effectively quantify T cell adhesion using flow conditions.
08:39
Human T Lymphocyte Isolation, Culture and Analysis of Migration In Vitro
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Cited by 25 •
2010
T lymphocyte migration occurs during homing to lymphoid organs, exit from the vasculature, and entering into peripheral tissues. Here, we describe a protocol that can be used to analyze T lymphocyte migration in vitro.
12:59
Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
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Cited by 36 •
2013
With effector functions distinct from other T cell subsets, Th17 cells have been centrally implicated in inflammatory autoimmunity. This in vitro Th17 differentiation protocol provides a means to determine whether naïve CD4+ T lymphocytes can differentiate into Th17 cells, and to further examine their role in autoimmunity and host response.
06:44
Creation of Abdominal Adhesions in Mice
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Cited by 10 •
2016
Abdominal adhesions that form after surgery are a major cause of pain, infertility, and hospitalization and reoperation for small bowel obstruction. Our surgical procedure for creating abdominal adhesions in mice is a reliable tool to study the mechanisms underlying the formation of adhesions.
FAQs
Rolling provides a controlled early contact between T lymphocytes and vascular endothelium rather than immediate immobilization. Selectins and their ligands support this transient interaction, allowing the cells to remain associated with the vessel while subsequent signals regulate the transition toward stronger adhesion. This staged behavior helps coordinate immune surveillance and movement toward sites where defense against infection is needed.
Chemokines act as activation signals that regulate integrin function on T lymphocytes. After chemokine-triggered activation, integrins such as LFA-1 can engage ICAM-1 more effectively, converting temporary contact into firm adhesion. This control is important because attachment must occur at the appropriate location and time, enabling lymphocytes to leave the circulation or establish productive contact with other immune cells.
The LFA-1 and ICAM-1 interaction supplies a strong adhesive connection after integrin activation. At vascular sites, it supports stable attachment that can contribute to migration into infected tissues. On antigen-presenting cells, the same interaction helps maintain close cell-cell contact and supports formation of an immunological synapse, where antigen recognition and signaling can proceed.
Adhesion coordinates where T lymphocytes can act rather than simply keeping them in circulation. Interactions with endothelium help guide cells toward infected tissues, while interactions with antigen-presenting cells stabilize contacts required for recognition and signaling. Consequently, defects or altered regulation in these adhesive steps can affect immune surveillance, tissue access, and the effectiveness of host defense.
Investigating the selectin, chemokine, integrin, and ICAM-1 interactions provides a framework for examining how lymphocytes are directed during inflammatory responses. In infection research, these adhesion events can be considered in relation to access to infected tissues and contact with antigen-presenting cells. This makes the process relevant to studying host-pathogen interactions and the cellular basis of immune defense.
Because adhesion controls tissue entry and stable immune-cell contacts, disrupted regulation can contribute to immune deficiencies by limiting surveillance or access to infected sites. Conversely, modifying these interactions offers a way to influence leukocyte trafficking. Studying the process therefore connects basic adhesion mechanisms with research on inflammatory disease, impaired host defense, and therapies designed to change immune-cell movement.