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Updated: Sep 20, 2026

Static Adhesion Assay for the Study of Integrin Activation in T Lymphocytes
Published on: June 13, 2014
Overlapping and selective roles of endothelial intercellular adhesion molecule-1 (ICAM-1) and ICAM-2 in lymphocyte
Joachim C U Lehmann1, Dorothee Jablonski-Westrich, Uta Haubold
1Experimentelle Rheumatologie, Universitätsklinik Charité, Humboldt-Universität and Deutsches Rheumaforschungszentrum, Schumannstrasse 21/22, 10117 Berlin, Germany.
Insights
Intercellular Adhesion Molecules (ICAMs) play roles in lymphocyte movement. ICAM-1 is crucial for trapping lymphocytes in the lung and migration to inflamed skin, while ICAM-1 and ICAM-2 have overlapping functions in lymph node recirculation.
Area of Science:
- Immunology
- Cellular Biology
- Molecular Medicine
Background:
- Integrin LFA-1 (leukocyte function-associated antigen 1) interacts with ICAMs (Intercellular Adhesion Molecules).
- ICAM-1 and ICAM-2 are expressed on endothelial cells and act as counterreceptors for lymphocytes.
- Understanding their roles is vital for modulating lymphocyte trafficking in immune responses.
Purpose of the Study:
- To investigate the distinct and overlapping roles of ICAM-1 and ICAM-2 in lymphocyte recirculation.
- To determine their contribution to lymphocyte recruitment into the lung and inflamed skin.
Main Methods:
- Utilized blocking monoclonal antibodies (mAbs) against ICAM-1 and ICAM-2.
- Employed mice genetically deficient for ICAM-1.
- Analyzed lymphocyte entry into lymph nodes, lung trapping, and skin migration.
Main Results:
- Lymphocyte entry into lymph nodes was not significantly affected by the absence of either ICAM-1 or ICAM-2 alone.
- Combined blockade of ICAM-1 and ICAM-2 markedly reduced lymphocyte recirculation through lymph nodes.
- ICAM-1 exclusively mediated LFA-1-dependent lymphocyte trapping in the lung.
- ICAM-1, but not ICAM-2, was essential for T effector cell migration into inflamed skin.
Conclusions:
- ICAM-1 and ICAM-2 exhibit redundant functions in lymphocyte recirculation via lymph nodes.
- ICAM-1 plays a unique and critical role in LFA-1-mediated lymphocyte sequestration in the lung.
- ICAM-1 is indispensable for T cell homing to sites of inflammation, such as inflamed skin.
Abstract:
The integrin LFA-1 interacts with a variety of ligands termed ICAMs. ICAM-1 and ICAM-2 are both expressed on endothelium and serve as counterreceptors during lymphocyte trafficking. In this study, we analyzed their relative contribution to lymphocyte recirculation through lymph nodes and to recruitment into lung and inflamed skin by blocking mAbs against ICAM-1 and ICAM-2 and mice deficient for ICAM-1. The entry of lymphocytes into peripheral and mesenteric lymph nodes was found to be unaffected by the functional deletion of either ICAM-1 or ICAM-2. However, when both pathways were blocked, recirculation through lymph nodes was strongly reduced. Trapping of lymphocytes in the lung after i.v. injection is partly mediated by LFA-1/ICAM interactions; the data presented in this study show an exclusive role of ICAM-1 in LFA-1-dependent lung trapping. Similarly, ICAM-1, but not ICAM-2, was required for the migration of T effector cells into the inflamed skin. These results indicate that ICAM-1 and ICAM-2 have redundant functions in lymphocyte recirculation through lymph nodes, but ICAM-1 is unique in supporting migration into inflamed sites and trapping within the lung.
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