The Involvement of Glial Cells in Blood-Brain Barrier Damage in Neuroimmune Diseases

Abstract

The blood-brain barrier and glial cells, particularly astrocytes, interact with each other in neuroimmune diseases. In the inflammatory environment typical of these diseases, alterations in vascular endothelial cell surface molecules and weakened cell connections allow immune cells and autoantibodies to enter the central nervous system. Glial cells influence the adhesion of endothelial cells by changing their morphology and releasing various signaling molecules. Multiple sclerosis has been the most studied disease in relation to vascular endothelial and glial cell interactions, but these cells also significantly affect the onset and severity of other neuroimmune conditions, including demyelinating and inflammatory diseases. In this context, we present an overview of these interactions and highlight how they vary across different neuroimmune diseases.

Keywords: astrocyte; blood–brain barrier; chemokine; cytokine; endothelial cell; microglia; multiple sclerosis; pericyte.

Figure 1

Interactions between the BBB and glial cells. Glial cells have either protective or disruptive effects, or both, on the BBB. Abbreviations: bFGF, basic fibroblast growth factor; ApoE, apolipoprotein E; S1P, sphingosine 1-phosphate; Slc4a4, solute carrier family 4 member 4; CCL, CC chemokine ligand; IL, interleukin; Shh, sonic hedgehog; RA, retinoic acid; PRDX, peroxiredoxin; Cx, connexin; HMGB, high mobility group box; VEGF, vascular endothelial growth factor; TYMP, thymidine phosphorylase; ATP, adenosine triphosphate; EphA4, ephrin A4; TNF, tumor necrosis factor; ROS, reactive oxygen species; TREM, triggering receptor of myeloid cells; Ang, angiotensin; MIF, migration inhibitory factor; ECs, endothelial cells.