EphA2 contributes to disruption of the blood-brain barrier in cerebral malaria

Thayer K. Darling, Patrice N. Mimche, Christian Bray, Banlanjo Umaru, Lauren M. Brady, Colleen Stone, Carole Else Eboumbou Moukoko, Thomas E. Lane, Lawrence S. Ayong, Tracey J. Lamb

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)


Disruption of blood-brain barrier (BBB) function is a key feature of cerebral malaria. Increased barrier permeability occurs due to disassembly of tight and adherens junctions between endothelial cells, yet the mechanisms governing junction disassembly and vascular permeability during cerebral malaria remain poorly characterized. We found that EphA2 is a principal receptor tyrosine kinase mediating BBB breakdown during Plasmodium infection. Upregulated on brain microvascular endothelial cells in response to inflammatory cytokines, EphA2 is required for the loss of junction proteins on mouse and human brain microvascular endothelial cells. Furthermore, EphA2 is necessary for CD8+ T cell brain infiltration and subsequent BBB breakdown in a mouse model of cerebral malaria. Blocking EphA2 protects against BBB breakdown highlighting EphA2 as a potential therapeutic target for cerebral malaria.

Original languageEnglish
Article numbere1008261
JournalPLoS Pathogens
Issue number1
Publication statusPublished - 2020
Externally publishedYes

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Molecular Biology
  • Genetics
  • Virology


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