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Updated: Jun 20, 2026

Static Adhesion Assay for the Study of Integrin Activation in T Lymphocytes
Published on: June 13, 2014
Junctional adhesion molecule (JAM)-B supports lymphocyte rolling and adhesion through interaction with alpha4beta1
Ralf J Ludwig1, Katja Hardt, Max Hatting
1Department of Dermatology, Clinic of the J.W. Goethe University, Frankfurt am Main, Germany. ralf.ludwig@uk-sh.de
Junctional adhesion molecule-B (JAM-B) facilitates leukocyte rolling and firm adhesion to endothelial cells, impacting immune cell extravasation. Blocking JAM-B significantly reduced leukocyte interactions and immune responses in vivo.
Area of Science:
- Immunology
- Cell Biology
- Vascular Biology
Background:
- Junctional adhesion molecule-A (JAM-A), JAM-B, and JAM-C are implicated in leukocyte transmigration.
- JAM-B binds to very late activation antigen (VLA)-4, a leukocyte integrin involved in lymphocyte adhesion to endothelial cells via vascular cell adhesion molecule (VCAM)-1.
Purpose of the Study:
- To investigate the role of JAM-B in leukocyte rolling and firm adhesion.
- To determine if JAM-B mediates leukocyte-endothelial interactions in vivo during immune responses.
Main Methods:
- Intravital microscopy of murine skin microvasculature to observe leukocyte rolling interactions.
- Dynamic flow chamber system to assess leukocyte rolling and sticking on JAM-B-coated slides.
- Adoptive transfer experiments in a 2,4,-dinitrofluorobenzene (DNFB)-induced contact hypersensitivity model.
Main Results:
- Blockade of JAM-B significantly reduced leukocyte rolling interactions in vivo.
- JAM-B-dependent rolling and sticking of T lymphocytes were observed at low shear stress, dependent on alpha4 and beta1 integrin.
- JAM-B blockade during sensitization impaired the immune response in a DNFB-induced contact hypersensitivity model, reducing ear swelling by approximately 40%.
Conclusions:
- JAM-B contributes to leukocyte extravasation by facilitating rolling and adhesion, in addition to transmigration.
- JAM-B plays a significant role in immune cell trafficking during inflammatory responses.
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