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The Blood-brain Barrier

The Blood-brain Barrier

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Related Experiment Video

Updated: Jan 14, 2026

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

PD-1 Blockade-Induced DKK1 Expression by CD8+ T Cells Promotes Blood-Brain Barrier Permeabilization.

Abhilash Deo^1,2, Sapir Levin^1,2, Chen Buxbaum^1,2,3

¹Department of Cell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel.

Cancer Discovery

|January 12, 2026

Summary

This summary is machine-generated.

Anti-PD1 therapy can disrupt the blood-brain barrier (BBB) through DKK1-expressing T cells, impacting brain metastasis (BrM) treatment. Targeting this BBB vulnerability may improve immunotherapy efficacy for BrM.

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Last Updated: Jan 14, 2026

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Published on: November 8, 2017

Area of Science:

Neuro-oncology
Immunotherapy
Cancer Biology

Background:

Anti-PD1 therapy offers benefits for some brain metastasis (BrM) patients, but response heterogeneity suggests gaps in understanding the brain's immune environment.
Existing research lacks clarity on host-specific factors influencing variable responses to immune checkpoint inhibitors (ICIs) in BrM.

Purpose of the Study:

To investigate the host-driven determinants of variable responses to anti-PD1 therapy in brain metastasis.
To characterize the brain microenvironment's immune landscape and its interaction with anti-PD1 treatment.

Main Methods:

Single-cell RNA sequencing was employed to analyze the brain microenvironment in response to anti-PD1 therapy.
Mechanisms of blood-brain barrier (BBB) integrity modulation by anti-PD1 therapy were investigated.
Plasma DKK1 levels and MRI contrast enhancement were assessed in patients.

Main Results:

Anti-PD1 therapy induced significant anti-tumor immune activation but uniquely compromised BBB integrity.
Activated CD8+ T cells expressing DKK1 were identified as mediators of BBB permeabilization via specific molecular pathways.
Clinical data showed increased MRI contrast enhancement in patients receiving anti-PD1, correlating DKK1 levels with BrM incidence in non-responders.
Combination therapy with anti-PD1 and cisplatin enhanced drug delivery and efficacy in ICI-resistant BrM.

Conclusions:

Anti-PD1 therapy can modulate BBB integrity, presenting a potential vulnerability in brain metastasis management.
Targeting DKK1-mediated BBB disruption offers a novel therapeutic strategy to enhance immunotherapy efficacy for brain metastases.
Sequential anti-PD1 and cisplatin therapy shows promise for overcoming ICI resistance in BrM.