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Related Experiment Video

Updated: Jun 18, 2026

Analysis of Lymphocyte Extravasation Using an In Vitro Model of the Human Blood-brain Barrier

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Published on: April 5, 2017

T lymphocytes impair P-glycoprotein function during neuroinflammation.

Gijs Kooij¹, Jack van Horssen, Elizabeth C M de Lange

¹Department of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands.

Journal of Autoimmunity

|December 5, 2009

Summary

Neuroinflammation impairs blood-brain barrier P-glycoprotein (P-gp) function, crucial for brain protection. Activated T cells, via ICAM-1 and NF-kappaB, reduce P-gp, potentially worsening brain diseases like multiple sclerosis.

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Published on: January 30, 2014

Area of Science:

Neuroscience
Immunology
Pharmacology

Background:

P-glycoprotein (P-gp; ABCB1) is vital for blood-brain barrier (BBB) function, protecting the central nervous system (CNS).
Optimal P-gp function maintains brain homeostasis by limiting entry of harmful substances.

Purpose of the Study:

To investigate the impact of neuroinflammation on vascular P-gp expression and function.
To elucidate the mechanisms by which T cells affect P-gp at the BBB.

Main Methods:

Utilized experimental allergic encephalomyelitis (EAE), an animal model for multiple sclerosis (MS).
Assessed P-gp expression and function in brain endothelial cells.
Investigated the role of CD4(+) T cells, ICAM-1, and NF-kappaB signaling.

Main Results:

P-gp expression and function were significantly decreased in EAE models and MS lesions.
Decreased P-gp correlated with perivascular T cell infiltrates.
Activated CD4(+) T cells, through ICAM-1 and NF-kappaB, induced P-gp malfunction.

Conclusions:

CD4(+) T cells impair endogenous protective mechanisms of the brain endothelium.
Loss of P-gp function during neuroinflammation may exacerbate CNS diseases by increasing exposure to toxins.
This study reveals a novel mechanism of P-gp dysfunction in neuroinflammatory conditions.