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The Fabp5/calnexin complex is a prerequisite for sensitization of mice to experimental autoimmune encephalomyelitis
Author(s) -
Paskevicius Tautvydas,
Jung Joanna,
Pujol Myriam,
Eggleton Paul,
Qin Wenying,
Robinson Alison,
Gutowski Nick,
Holley Janet,
Smallwood Miranda,
Newcombe Jia,
Zochodne Douglas,
Chen XingZhen,
Tang Jingfeng,
Kraus Allison,
Michalak Marek,
Agellon Luis B.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.202001539rr
Subject(s) - experimental autoimmune encephalomyelitis , calnexin , sensitization , immunology , encephalomyelitis , medicine , multiple sclerosis , biology , microbiology and biotechnology , endoplasmic reticulum , calreticulin
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.