| First Author | Paskevicius T | Year | 2020 |
| Journal | FASEB J | Volume | 34 |
| Issue | 12 | Pages | 16662-16675 |
| PubMed ID | 33124722 | Mgi Jnum | J:313320 |
| Mgi Id | MGI:6705451 | Doi | 10.1096/fj.202001539RR |
| Citation | Paskevicius T, et al. (2020) The Fabp5/calnexin complex is a prerequisite for sensitization of mice to experimental autoimmune encephalomyelitis. FASEB J 34(12):16662-16675 |
| abstractText | We previously showed that calnexin (Canx)-deficient mice are desensitized to experimental autoimmune encephalomyelitis (EAE) induction, a model that is frequently used to study inflammatory demyelinating diseases, due to increased resistance of the blood-brain barrier to immune cell transmigration. We also discovered that Fabp5, an abundant cytoplasmic lipid-binding protein found in brain endothelial cells, makes protein-protein contact with the cytoplasmic C-tail domain of Canx. Remarkably, both Canx-deficient and Fabp5-deficient mice commonly manifest resistance to EAE induction. Here, we evaluated the importance of Fabp5/Canx interactions on EAE pathogenesis and on the patency of a model blood-brain barrier to T-cell transcellular migration. The results demonstrate that formation of a complex comprised of Fabp5 and the C-tail domain of Canx dictates the permeability of the model blood-brain barrier to immune cells and is also a prerequisite for EAE pathogenesis. |
