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Updated: Aug 10, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Lymphocyte migration into the central nervous system: implication of ICAM-1 signalling at the blood-brain barrier
John Greenwood1, Sandrine Etienne-Manneville, Peter Adamson
1Institute of Ophthalmology, University College London, Bath Street, London EC1V 9EL, UK.
Insights
Intercellular Adhesion Molecule-1 (ICAM-1) signaling in brain endothelial cells is crucial for lymphocyte entry into the central nervous system (CNS). This process impacts neuroinflammation and diseases like multiple sclerosis.
Area of Science:
- Neuroimmunology
- Vascular Biology
- Cellular Signaling
Background:
- Lymphocyte recruitment to the CNS is vital in neuroinflammatory diseases like multiple sclerosis.
- The vascular endothelium's role in lymphocyte transvascular migration is increasingly recognized.
- Adhesion molecules, such as ICAM-1, act as ligands and signal transducers.
Purpose of the Study:
- To review current understanding of endothelial cell ICAM-1 signaling.
- To discuss the significance of ICAM-1 signaling in leukocyte trafficking to the CNS.
- To highlight ICAM-1's role in the multistep paradigm of leukocyte recruitment.
Main Methods:
- Review of existing literature on endothelial cell signaling and leukocyte recruitment.
- Analysis of the role of immunoglobulin superfamily adhesion molecules.
- Focus on ICAM-1-mediated signaling pathways in brain endothelial cells.
Main Results:
- Adhesion molecules, including ICAM-1, initiate endothelial signaling cascades.
- ICAM-1 signaling in brain endothelial cells is a critical regulatory step for lymphocyte migration across the blood-brain barrier.
- This signaling influences downstream effector mechanisms impacting neuroinflammation.
Conclusions:
- Endothelial ICAM-1 signaling represents a key phase in leukocyte recruitment to the CNS.
- Understanding ICAM-1's role is crucial for developing therapeutic strategies for CNS diseases.
- Targeting ICAM-1 signaling may modulate lymphocyte trafficking and neuroinflammation.
Abstract:
Lymphocyte recruitment to the central nervous system (CNS) is a critical step in the pathogenesis of diseases such as multiple sclerosis (MS), meningitis and posterior uveitis. The principle sequential stages that control lymphocyte emigration from the blood have been widely reported, but only recently has attention been directed towards the role of the vascular endothelium in actively supporting transvascular migration. It has now been shown that adhesion molecules, particularly those of the immunoglobulin super family (e.g. ICAM-1, VCAM-1 and PECAM-1), not only act as ligands for leucocyte receptors but can also serve as signal transducers. Engagement of these receptors initiates endothelial signalling cascades that result in downstream effector mechanisms which in turn influence the progression of neuroinflammation. In particular, it has been shown that ICAM-1-mediated signalling in brain endothelial cells is a crucial regulatory step in the process of lymphocyte migration through the blood-brain barrier and as such represents an additional phase in the multistep paradigm of leucocyte recruitment. In this article we review current understanding of endothelial cell ICAM-1 signalling and discuss the importance of these findings in relation to leucocyte trafficking to the CNS.
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